PVFS/ME/CFS Watch

Research paper: CFS, the immune system and viral infection, 2 July 2011

noreply@blogger.com (Ingrid J. Jones) — Tue, 19 Jul 2011 10:54:00 +0000

From the M.E. Association's website, a post by Tony Britton entitled 'Research paper: CFS, the immune system and viral infection, 2 July 2011':

From Brain, Behaviour and Immunity, the official journal of the Psychoneuroimmunology Research Society (PNIRS). 2011 Jul 2. [Epub ahead of print]

Chronic fatigue syndrome, the immune system and viral infection.

Bansal AS, Bradley AS, Bishop KN, Kiani S, Ford B.
Dept. of Immunology, Epsom and St. Helier University Hospitals NHS Trust, Carshalton, Surrey, SM5 1AA and Chronic Illness Research Team, Stratford Campus, University of East London, London E15 4LZ, UK.

Abstract

The chronic fatigue syndrome (CFS), as defined by recent criteria, is a heterogeneous disorder with a common set of symptoms that often either follows a viral infection or a period of stress. Despite many years of intense investigation there is little consensus on the presence, nature and degree of immune dysfunction in this condition. However, slightly increased parameters of inflammation and pro-inflammatory cytokines such as interleukin (IL) 1, IL6 and tumour necrosis factor (TNF) α are likely present. Additionally, impaired natural killer cell function appears evident. Alterations in T cell numbers have been described by some and not others. While the prevalence of positive serology for the common herpes viruses appears no different from healthy controls, there is some evidence of viral persistence and inadequate containment of viral replication. The ability of certain herpes viruses to impair the development of T cell memory may explain this viral persistence and the continuation of symptoms. New therapies based on this understanding are more likely to produce benefit than current methods.

Copyright © 2011. Published by Elsevier Inc.

PMID: 21756995 [PubMed - as supplied by publisher]

What's it like to have severe ME/CFS? It's a living death and hell in solitary confinement

noreply@blogger.com (Ingrid J. Jones) — Thu, 14 Jul 2011 08:05:00 +0000

BEFORE a viral illness struck me down in 1999, I never imagined that such a disabling and painful illness could exist without it being taken seriously by British doctors and health care professionals.

It's a lonely feeling and tough to take when you see the scepticism in their eyes and/or hear it in their voices. When they don't take M.E. seriously how are others, family and friends, expected to understand or even believe us?

Watching the following excellent video from getwellfromme.com entitled "What is it like to have M.E.?" made me cry.

Today, my answer to the question "What is it like to have severe M.E.?" would be this: "It's a living death and hell in solitary confinement".

Tomorrow, I might be feeling worse but my answer to the question would still be the same because every day is bad.

Some days even are worse if I do too much, other days are horrendous for months on end if I get an infection or go out.

I've been too ill to sit up long enough to go out in a wheelchair and manage the basics of day to day life after I return home.

Hopefully, now that I am on painkillers which are helping me to control some of the symptoms, next year will be different.

If you, or any person you know or care for, are suffering from severe M.E., please contact the The 25% M.E. Support Group, the UK's only national support group for people severely affected by M.E. (c. 25% of M.E. sufferers are severely affected, hence the name).

There are two separate forms of Membership in order to try to provide a suitable service for as many sufferers as possible, whether severely, moderately or mildly affected by ME and, of course also provide support to carers of ME sufferers.

Credit: Video courtesy of getwellfromme.com
Hat tip: Rachel M @bluecoffeemug / YouTube http://youtu.be/qBriPTFOtmY (read comments)

New study: Gene expression alterations at baseline and following moderate exercise in patients with CFS & FMS

noreply@blogger.com (Ingrid J. Jones) — Tue, 14 Jun 2011 22:48:00 +0000

RESEARCHERS behind a new study say they've discovered post-exercise differences in genetic expression that meet criteria for an objective biomarker for a subgroup of chronic fatigue syndrome (ME/CFS). They also say data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls. Further details in three reports reprinted here below.

(1) From Post Viral Fatigue Forum, 6 June 2011 www.postviralfatigue.me.uk Full copy:

New Study Claims Change in Gene Expression in CFS

Looks interesting: http://chronicfatigue.about.com/b/2011/06/06/genetic-expression-after-exercise-in-fibromyalgia-chronic-fatigue-syndrome.htm

Researchers analyzed blood samples before exercise to get a baseline, then took samples again half an hour, 8 hours, 24 hours and 48 hours after moderate exercise.

They found that:

- 71% of the ME/CFS group (34 of 48) had increased expression of 4 genes dealing with sensory and adrenergic receptors and cytokines for 48 hours after exercise; Those with the largest change in genetic expression also had the largest increase in post-exercise symptoms.

- The other 29% of the ME/CFS group (14 of 48) did not show the above changes but did have a decrease in expression of the adrenergic α-2A receptor; This group had significantly more orthostatic intolerance (dizziness upon standing) than the first group.

- Healthy controls and people with FMS had no post-exercises changes in the genes that were studied.

They [the researchers] say the data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls.

Seems encouraging to me.

B.
edited by Barbarian on 6/6/2011 [End]

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(2) From About.com Guide Fibromyalgia & Chronic Fatigue
6 June 2011 - http://chronicfatigue.about.com
By Adrienne Dellwo
Full copy:

Research Brief

Researchers behind a new study [full copy below, courtesy of PubMed] say they've discovered post-exercise differences in genetic expression that meet criteria for an objective biomarker for a subgroup of chronic fatigue syndrome (ME/CFS). They also say data show two distinct subgroups of ME/CFS and also differentiate fibromyalgia (FMS) from both ME/CFS and healthy controls.

Researchers analyzed blood samples before exercise to get a baseline, then took samples again half an hour, 8 hours, 24 hours and 48 hours after moderate exercise (maintaining maximum heart rate for 20 minutes.) They were looking for changes in genes that deal with sensory fatigue and muscle pain, which are common post-exercise symptoms of ME/CFS. The found that:

71% of the ME/CFS group (34 of 48) had increased expression of 4 genes dealing with sensory and adrenergic receptors and cytokines for 48 hours after exercise;
Those with the largest change in genetic expression also had the largest increase in post-exercise symptoms;

The other 29% of the ME/CFS group (14 of 48) did not show the above changes but did have a decrease in expression of the adrenergic α-2A receptor;
This group had significantly more orthostatic intolerance (dizziness upon standing) than the first group;

Healthy controls and people with FMS had no post-exercises changes in the genes that were studied;
However, those with FMS had baseline elevations in 3 genes -- 2 sensory ion channels and 1 cytokine -- that were not found in the other groups.
These differences in genetic expression could help explain post-exertional malaise (PEM), which is considered the hallmark symptom of ME/CFS. PEM causes a marked upswing in symptoms after exertion, and for some people it takes very little exertion -- such as taking a shower or walking to the mailbox -- to trigger this symptom. In the most severe cases, even sitting up for a few minutes can lead to PEM.

FMS involves a similar but generally less-severe reaction to over exertion or stressful events, and these genetic abnormalities could help shed light on this as well.

Researchers concluded that these findings could help establish an objective biomarker for diagnosing at least 1 subgroup of ME/CFS, guide treatment for both identified ME/CFS subgroups, and differentiate FMS from ME/CFS. [End]

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(3) From PubMed - May 2011 - National Center for Biotechnology Information, U.S. National Library of Medicine
http://www.ncbi.nlm.nih.gov/pubmed/21615807?forumid=331851
Full copy:

J Intern Med. 2011 May 26. doi: 10.1111/j.1365-2796.2011.02405.x. [Epub ahead of print]

Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.

Light AR, Bateman L, Jo D, Hughen RW, Vanhaitsma TA, White AT, Light KC.

Source
Department of Anesthesiology, University of Utah, Salt Lake City, UT The Brain Institute, University of Utah, Salt Lake City, UT Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT Department of Exercise and Sprt Science, University of Utah, Salt Lake City, UT.

Abstract
Light AR, Bateman L, Jo D, Hughen RW, VanHaitsma TA, White AT, Light KC (University of Utah Dept. Anesthesiology, Dept. Neurobiology and Anatomy, Dept. Exercise and Sport Science) Gene expression alterations at baseline and following moderate exercise in patients with Chronic Fatigue Syndrome, and Fibromyalgia Syndrome.

Objectives: To determine mRNA expression differences in genes involved in signaling and modulating sensory fatigue, and muscle pain in patients with Chronic Fatigue Syndrome (CFS) and Fibromyalgia Syndrome (FM) at baseline, and following moderate exercise.

Design: Forty eight Patients with CFS-only, or CFS with comorbid FM, 18 Patients with FM that did not meet criteria for CFS, and 49 healthy Controls underwent moderate exercise (25 minutes at 70% maximum age predicted heart-rate). Visual-analogue measures of fatigue and pain were taken before, during, and after exercise. Blood samples were taken before, and 0.5, 8, 24, and 48 hours after exercise. Leukocytes were immediately isolated from blood, number coded for blind processing and analyses, and flash frozen. Using real-time, quantitative PCR, the amount of mRNA for 13 genes (relative to control genes) involved in sensory, adrenergic, and immune functions was compared between groups at baseline, and following exercise. Changes in amounts of mRNA were correlated with behavioral measures, and functional clinical assessments.

Results: No gene expression changes occurred following exercise in Controls. In 71% of CFS patients, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48 hours. These post-exercise increases correlated with behavioral measures of fatigue and pain. In contrast, for the other 29% of CFS patients, adrenergic α-2A receptor's transcription was decreased at all time points after exercise; other genes were not altered. History of orthostatic intolerance was significantly more common in the α-2A decrease subgroup. FM only patients showed no post-exercise alterations in gene expression, but their pre-exercise baseline mRNA for two sensory ion channels and one cytokine were significantly higher than Controls.

Conclusions: At least two subgroups of CFS patients can be identified by gene expression changes following exercise. The larger subgroup showed increases in mRNA for sensory and adrenergic receptors and a cytokine. The smaller subgroup contained most of the CFS patients with orthostatic intolerance, showed no post-exercise increases in any gene, and was defined by decreases in mRNA for α-2A. FM only patients can be identified by baseline increases in 3 genes. Post-exercise increases for 4 genes meet published criteria as an objective biomarker for CFS, and could be useful in guiding treatment selection for different subgroups.

Copyright © 2011 The Association for the Publication of the Journal of Internal Medicine.

PMID: 21615807 [PubMed - as supplied by publisher] [End]

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The US National Institutes of Health is sponsoring new studies to ascertain whether the association between XMRV and CFS can be confirmed

noreply@blogger.com (Ingrid J. Jones) — Thu, 09 Jun 2011 10:27:00 +0000

Dr Jonathan Stoye, a retrovirologist at the UK Medical Research Council National Institute for Medical Research, has joined in criticism of the XMRV paper by Lombardi and colleagues, despite having co-written an editorial in Science in 2009 in support of it.

Dr Stoye said it should not be forgotten that a subset of CFS patients “almost certainly” had disease triggered by a viral infection, and although efforts to explain this should continue, the viral trigger was not XMRV.

The US National Institutes of Health is sponsoring new studies to ascertain whether the association between XMRV and CFS can be confirmed.

Editor in chief of Science, Bruce Alberts, writing in the journal, said, “Science eagerly awaits the outcomes of these further studies and will take appropriate action when their results are known.”

Full story below from MEA website June 8, 2011:

‘Science asks researchers to withdraw paper on chronic fatigue syndrome and infectious retrovirus’, British Medical Journal, 6 June 2011

From the British Medical Journal, 6 June 2011 (news story by Matthew Limb)

Researchers are facing calls to retract published findings that link chronic fatigue syndrome to a retrovirus called xenotropic murine leukemia virus related virus (XMRV) after new scientific criticism of their validity.

Editors of the journal, Science, have issued an “editorial expression of concern” over a research paper it published in October 2009, saying the report is “now seriously in question.”

The study, “Detection of an infectious retrovirus, XMRV, in blood cell of patients with chronic fatigue syndrome,” was led by Vincent Lombardi and Judy Mikovits of the Whittemore Peterson Institute, Reno, Nevada (Science 2009;326:585).

It purported to show that a retrovirus XMRV was present in the blood of 67% of patients with chronic fatigue syndrome (CFS) compared with 3.7% of healthy controls.

The study caused a stir when it appeared and led to some CFS patients, believing XMRV to be a possible contributor to their condition, seeking antiretroviral treatments marketed to combat HIV.

But Science, which is the weekly journal of the American Association for the Advancement of Science, has now highlighted “flaws” in the paper.

Since 2009, it says, at least 10 studies conducted by other investigators and published elsewhere have failed to detect XMRV in independent populations of CFS patients.

Furthermore, Science has published two new reports that “strongly support the growing view that the association between XMRV and CFS described by Lombardi and colleagues likely reflects contamination of laboratories and research reagents with the virus.”

One report provides evidence that the virus originated when two mouse leukaemia viruses underwent recombination during experimental passage of a human prostate tumour xenograft in mice in the 1990s.

In their analysis, Paprotka and colleagues conclude that laboratory contamination with XMRV produced by a cell line (22Rv1) derived from these early xenograft experiments is the most likely explanation for detection of the virus in patient samples. (Science 2011 doi:10.1126/science.1205292)

“Our results suggest that the association with XMRV with human disease is due to contamination of human samples with virus originating from this recombination event,” the authors write.

In the second report, K Knox and colleagues examined blood samples from 61 CFS patients from the same medical practice that had provided patient samples to Lombardi and colleagues.

Comprehensive assays by Knox and colleagues for viral nucleic acids, infectious virus, and virus-specific antibodies showed no evidence of XMRV in any of the samples (Science 2011 doi:10.1126/science.1204963).

In February 2010, a Dutch study refuting the original US study reporting the link was published in the BMJ (2010;341:c1018; doi:10.1136/bmj.c1018).

It has emerged that editors of Science, before publishing their “editorial expression of concern,” privately requested that the authors of the original study retract it themselves.

Dr Judy Mikovits has written to the editors warning that Science’s action could be “disastrous” for future research in this field while insisting the study is accurate.

She wrote that she and her co-authors shared the “deep concern” over the number of studies that had not been able to replicate their findings.

She said other scientists had not replicated their work faithfully and there were no data to support claims of laboratory contamination.

Since the study was published there have been calls in the US for people with CFS to be barred from donating blood in case blood supplies might be contaminated by the “contagious” retrovirus.

The US National Institutes of Health is sponsoring new studies to ascertain whether the association between XMRV and CFS can be confirmed.

Editor in chief of Science, Bruce Alberts, writing in the journal, said, “Science eagerly awaits the outcomes of these further studies and will take appropriate action when their results are known.”

Jonathan Stoye, a retrovirologist at the UK Medical Research Council National Institute for Medical Research, has joined in criticism of the paper by Lombardi and colleagues, despite having co-written an editorial in Science in 2009 in support of it.

He told the BMJ that there was strong evidence that contamination explained the findings and therefore the suggested the link between XMRV and CFS was “wrong.”

He said, “Nobody has reproduced the original results and that is very unsatisfactory.” I don’t see any reasons for the scientific community to spend any more time and effort on this.”

He told the BMJ he had no plans to do further research himself in this area, adding, “I believe the scientific argument is done, but the political argument may not be.”

He said although requests to withdraw a published research paper were “unusual, it does happen.

“In football terms, it’s somewhere between a yellow and a red card,” he said.

Dr Stoye said it should not be forgotten that a subset of CFS patients “almost certainly” had disease triggered by a viral infection, and although efforts to explain this should continue, the viral trigger was not XMRV.

Charles Shepherd, medical adviser to the UK based ME Association, a national charity supporting people affected by myalgic encephalopathy (ME), CFS, and post viral fatigue syndrome, said the failure of many leading experts to support the findings of Lombardi and colleagues “must be taken seriously.”

He said the charity was waiting to hear the results of ongoing US research, including a multicentre study of CFS patients by virologist Ian Lipkin, which might provide “definitive” results.

Dr Shepherd told the BMJ, “I am trying to take a balanced view although it will be a tremendous disappointment to many patients if it turns out that XMRV is a red herring.”

He said, given the current uncertainty, it would be “unethical” for doctors to prescribe antiretrovirals for CFS patients, and there was no evidence for this happening in the UK.

Peter Spencer, chief executive of the charity Action for ME, said, “Like many patients, we were excited when the original study was published in 2009, and hoped that further studies would lead to independent and substantive confirmation of a link between XMRV and ME. Unfortunately, it seems that it is now time to move on. But it’s imperative that this very disappointing news does not overshadow the continuing importance of rigorous scientific study into the biology of ME. There is still a long way to go.”

Viral Encephalomyelitis - Academic review

noreply@blogger.com (Ingrid J. Jones) — Thu, 07 Apr 2011 11:20:00 +0000

ENCEPHALOMYELITIS is an unusual complication of infection with encephalitic viruses.

The term encephalomyelitis refers to inflammation in the brain and spinal cord that results from the immune response to virus infection. In humans, the viruses most commonly identified as causes of viral encephalomyelitis include herpesviruses and RNA viruses in the enterovirus, e.g., polio, enterovirus 71.

The primary target cells for most encephalitic viruses are neurons, although a few viruses attack cerebrovascular endothelial cells to cause ischemia and stroke or glial cells to cause demyelination, encephalopathy, or dementia.

Widespread infection of neurons may occur or viruses may display preferences for particular types of neurons in specific locations in the central nervous system (CNS). For instance, herpes simplex virus (HSV) type 1 often infects neurons in the hippocampus to cause behavioral changes, while poliovirus preferentially infects motor neurons in the brainstem and spinal cord to cause paralysis and Japanese encephalitis virus infects basal ganglia neurons to cause symptoms similar to those of Parkinson’s disease.

Because infections with encephalitic viruses are initiated outside the CNS (e.g., with an insect bite, skin, respiratory, or gastrointestinal infection), innate and adaptive immune responses are usually mounted rapidly enough to prevent virus entry into the CNS. Therefore, most viruses that can cause encephalitis more often cause asymptomatic infection or a febrile illness without neurologic disease, and encephalomyelitis is an uncommon complication of infection.

Full details below.

Useful academic review of encephalomyelitis: PLoS Pathogens
Source: ME Association website posted by Tony Britton
April 7, 2011. Copy in full:

From PLoS Pathogens, March 2011.

Diane E. Griffin*

W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America

Citation: Griffin DE (2011) Viral Encephalomyelitis. PLoS Pathog 7(3): e1002004. doi:10.1371/journal.ppat.1002004

Editor: Hiten D. Madhani, University of California San Francisco, United States of America

Published: March 24, 2011

Copyright: © 2011 Diane E. Griffin. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: Work from the author’s laboratory was supported by the NIH/NINDS (R01 NS038932) and the Dana Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The author has declared that no competing interests exist.

* E-mail: dgriffin@jhsph.edu

Encephalomyelitis Is an Unusual Complication of Infection with Encephalitic Viruses

Viral encephalomyelitis is an important cause of morbidity and mortality worldwide, and many encephalitic viruses are emerging and re-emerging due to changes in virulence, spread to new geographic regions, and adaptation to new hosts and vectors [1]. The term encephalomyelitis refers to inflammation in the brain and spinal cord that results from the immune response to virus infection. In humans, the viruses most commonly identified as causes of viral encephalomyelitis are herpesviruses and RNA viruses in the enterovirus (e.g., polio, enterovirus 71), rhabdovirus (e.g., rabies), alphavirus (e.g., eastern equine, Venezuelan equine, and western equine encephalitis), flavivirus (e.g., West Nile, Japanese encephalitis, Murray Valley, and tick-borne encephalitis), and bunyavirus (e.g., La Crosse) families. Other virus families with members that can cause acute encephalitis are the paramyxoviruses (e.g., Nipah, Hendra) and arenaviruses (e.g., lymphocytic choriomeningitis, Junin). However, this is certainly not a complete list, because for most cases of human viral encephalitis the etiologic agent is not identified, even when heroic attempts are made [2].

The primary target cells for most encephalitic viruses are neurons, although a few viruses attack cerebrovascular endothelial cells to cause ischemia and stroke or glial cells to cause demyelination, encephalopathy, or dementia [3]–[5]. Widespread infection of neurons may occur or viruses may display preferences for particular types of neurons in specific locations in the central nervous system (CNS). For instance, herpes simplex virus (HSV) type 1 often infects neurons in the hippocampus to cause behavioral changes, while poliovirus preferentially infects motor neurons in the brainstem and spinal cord to cause paralysis and Japanese encephalitis virus infects basal ganglia neurons to cause symptoms similar to those of Parkinson’s disease.

Because infections with encephalitic viruses are initiated outside the CNS (e.g., with an insect bite, skin, respiratory, or gastrointestinal infection), innate and adaptive immune responses are usually mounted rapidly enough to prevent virus entry into the CNS. Therefore, most viruses that can cause encephalitis more often cause asymptomatic infection or a febrile illness without neurologic disease, and encephalomyelitis is an uncommon complication of infection.

Encephalitic Viruses Can Use Neuronal or Non-Neuronal Pathways to Enter the CNS

When a virus does invade the CNS, there are several routes by which infection of neurons can occur. The most common entry point is from the blood, and the level of viremia as a result of virus replication in peripheral organs often correlates with the likelihood of CNS infection. However, the blood–brain barrier (BBB), composed of vascular endothelial cells with tight junctions in contact with the foot processes of astrocytes, inhibits direct access to the brain parenchyma and neurons. Some neurotropic viruses can replicate in cerebrovascular endothelial cells, enter with infected leukocytes, or cross directly into the cerebrospinal fluid (CSF) through the porous capillaries of the choroid plexus. A specialized CNS entry pathway used by several viruses, most notably HSV, varicella zoster, and rabies viruses, is by way of nerve terminals in peripheral organs. These viruses can enter the nerve and then use neural transport mechanisms to transport the infecting virions to the neuronal cell body where replication occurs [6], [7]. A variation on this theme is infection through the exposed end processes of neurons in the nasal olfactory epithelium, followed by transport of the virus to the olfactory lobe within the CNS. Intranasal infection is commonly used to initiate infection of the CNS in experimental animals, but in humans this pathway may be important only in rare cases of aerosol exposure to a neurotropic virus [8]–[10].

In tissue culture systems most of these viruses can infect many types of cells, in addition to neurons. Few neuron-specific virus receptors have been identified (e.g., p75NTR, NCAM, and AChR for rabies; nectin for HSV) but these do not always account for neuronotropism in vivo [11]–[13]. Recent studies with HSV suggest that receptors used to enter processes of peripheral neurons can be different from those used to infect neurons in the brain [12]. Therefore, the mechanisms by which encephalitic viruses target neurons to the exclusion of other cells within the CNS are poorly understood. Once within the nervous system, encephalitic viruses often follow synaptic pathways for spread to other neuronal populations. These viruses interact with motor proteins either directly or through accessory proteins to travel using both anterograde (kinesin motors) and retrograde (dynein-dynactin motors) neuronal microtubule transport systems [6].

Neuronal Damage Can Be Caused Directly by Virus Infection or by the Immune Response to the Infection

In addition to fever and headache, signs and symptoms of viral encephalomyelitis typically include evidence of neuronal dysfunction—seizures, cognitive impairment, ataxia, paralysis, etc. Virus replication can damage neurons directly by inducing cell death through apoptotic or necrotic mechanisms (Figure 1) [14]. Many viruses cause more severe CNS disease in the young. For these infections, immature neurons support more efficient virus replication and greater virus-induced cell death than mature neurons [15]. In humans, Venezuelan equine encephalitis and La Crosse viruses cause symptomatic neurologic disease almost exclusively in children, although adults are equally susceptible to infection [16], [17]. Conversely, for unexplained reasons, neurologic disease due to West Nile virus infection occurs primarily in people over the age of 60 years [18].
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Figure 1. Schematic diagram of the potential outcomes after virus infection of neurons.

Virus infection itself may induce death of the infected neuron, especially in young individuals. Neuronal death can also result from the local release of excitotoxic neurotransmitters (e.g., glutamate) and inflammatory mediators. Neurons can also survive infection and virus replication can be controlled through noncytolytic mechanisms such as local production of antiviral antibody and interferon (IFN)-γ. In the latter case, viral nucleic acid persists intracellularly and long-term immune control is necessary to prevent virus reactivation.
doi:10.1371/journal.ppat.1002004.g001

Although neuronal virus infection per se is necessary for, and contributes directly to, neuronal dysfunction, the inflammatory response in the CNS is also a major contributor to neuronal damage and can even result in death of nearby uninfected neurons (Figure 1) [19], [20]. The CNS inflammatory response to virus infection consists of activation and proliferation of resident astrocytes and microglial cells and of perivascular and parenchymal infiltration of activated monocytes and lymphocytes from the blood. The mechanism(s) by which the immune response causes neuronal damage are incompletely understood, but evidence exists for production of neurotoxins and reactive oxygen and nitrogen species by activated glial cells, increased levels of the excitotoxic neurotransmitter glutamate, and production of cytokines by activated lymphocytes [21]. The ability to control inflammation through induction of regulatory T cells and suppression of lymphocyte function by infected neurons can be an important determinant of outcome [22], [23]. In alphavirus encephalomyelitis, combined prevention of inflammation and glutamate excitotoxicity by treatment with glutamate receptor antagonists prevents paralysis and death despite continued virus replication [20].

Virus Clearance from Neurons Is Complicated by the Irreplaceable Nature of Neurons

The immune response to infection can contribute to fatal disease, but is also necessary for recovery and virus clearance. Elimination of virus-infected cells from tissue requires elimination of all cells in which the virus is replicating. This can occur either by virus-induced or immune-mediated cytolysis. T cells are ideal for this purpose because they recognize viral antigen as processed antigen only in the context of cell surface–expressed MHC class I (CD8+ T cells) or of MHC class II (CD4+ T cells) and can possess cytotoxic properties. Neurons are long-lived essential cells that cannot be replaced, so a noncytolytic immune mechanism for virus clearance would be advantageous to the host to avoid death of surviving cells. If the immune clearance mechanism is damaging to the infected neuron, then the function of that neuron will be lost and the outcome for the host will be the same as if the virus infection had caused neuronal death.

Because mature neurons are relatively resistant to virus-induced cell death [15], noncytolytic mechanisms for virus clearance can be employed to control or eliminate infection. If infected cells are allowed to survive, the clearance of virus must include mechanisms for inhibiting intracellular synthesis of virus nucleic acid and protein, and for removing virus genomes from cells or preventing their replacement after degradation. Alphavirus encephalitis has been most thoroughly studied, and two noncytolytic clearance mechanisms have been identified: IFN-γ and anti-viral antibody (Figure 1). However, not all types of neurons are equally responsive to virus clearance by these mechanisms. IFN-γ acts through a Jak/STAT signaling pathway to activate an antiviral response that suppresses virus replication in motor neurons without toxicity, but the relevant antiviral proteins have not been identified [24]. Antibody to the E2 viral glycoprotein present on the surface of infected neurons suppresses virus replication in all populations of neurons through a pathway that requires bivalent antibody, but does not require complement or effector cells [25], [26].

Recovery from Encephalitis Results in Virus Persistence and the Need for Long-Term Immune Control

Because the noncytolytic process for virus clearance does not completely eliminate viral RNA from neurons, a mechanism for long-term immunologic control of virus replication is needed to prevent virus reactivation or progressive disease [27], [28]. Antibody is likely to participate in control, as well as initial clearance. Maintaining adequate levels of antibody in the CNS for continued control of virus replication requires either passage of antibody from the blood into the brain parenchyma or local production by resident antibody-secreting cells. The BBB restricts the entry of proteins from the blood into the CNS, and although this function is compromised during the acute phase of infection, it is quickly repaired. Under normal conditions, levels of antibody in the brain are sustained at 1% of plasma levels that are likely to be inadequate for long-term prevention of virus reactivation. Therefore, resident long-lived antibody-secreting cells that can continue to produce antiviral antibody for a lifetime are a feature of recovery from most CNS virus infections [29]. Long-term immune control of virus replication is not always successful, leading to recurrent or progressive neurologic disease [30]–[32].

Conclusions

Encephalomyelitis resulting from virus infection of neurons is a disease that can be fatal or result in permanent disability due to irreversible damage of infected neurons. The immune response to infection can enhance neuronal damage or can control virus replication by noncytolytic mechanisms and thus determine outcome. However, noncytolytic virus clearance results in persistence of viral nucleic acid in the CNS and thus establishes a need for long-term local immune responses to prevent reactivation of infection and progressive disease. Understanding these mechanisms is necessary for development of strategies for treating and preventing neurologic disease due to viral encephalomyelitis.

References

1. Griffin DE (2010) Emergence and re-emergence of viral diseases of the central nervous system. Prog Neurobiol 91: 95–101.

2. Glaser CA, Honarmand S, Anderson LJ, Schnurr DP, Forghani B, Cossen CK, Schuster FL, Christie LJ, Tureen JH (2006) Beyond viruses: clinical profiles and etiologies associated with encephalitis. Clin Infect Dis 43: 1565–1577.

3. Gilden D, Cohrs RJ, Mahalingam R, Nagel MA (2009) Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment. Lancet Neurol 8: 731–740.

4. Major EO (2010) Progressive multifocal leukoencephalopathy in patients on immunomodulatory therapies. Annu Rev Med 61: 35–47.

5. Takahashi K, Wesselingh S, Griffin DE, McArthur JC, Johnson RT, Glass JD (1996) Localization of HIV-1 in human brain using polymerase chain reaction/in situ hybridization and immunocytochemistry. Ann Neurol 39: 705–711.

6. Lyman MG, Enquist LW (2009) Herpesvirus interactions with the host cytoskeleton. J Virol 83: 2058–2066.

7. Ugolini G (2008) Use of rabies virus as a transneuronal tracer of neuronal connections: implications for the understanding of rabies pathogenesis. Dev Biol (Basel) 131: 493–506.

8. Thach DC, Kimura T, Griffin DE (2000) Differences between C57BL/6 and BALB/cBy mice in mortality and virus replication after intranasal infection with neuroadapted Sindbis virus. J Virol 74: 6156–6161.

9. Roy CJ, Reed DS, Wilhelmsen CL, Hartings J, Norris S, Steele KE (2009) Pathogenesis of aerosolized eastern equine encephalitis virus infection in guinea pigs. Virol J 6: 170. doi: 10.1186/1743-422X-6-170.

10. Yamada M, Nakamura K, Yoshii M, Kaku Y, Narita M (2009) Brain lesions induced by experimental intranasal infection of Japanese encephalitis virus in piglets. J Comp Pathol 141: 156–162.

11. Tuffereau C, Schmidt K, Langevin C, Lafay F, Dechant G, Koltzenburg M (2007) The rabies virus glycoprotein receptor p75NTR is not essential for rabies virus infection. J Virol 81: 13622–13630.

12. Kopp SJ, Banisadr G, Glajch K, Maurer UE, Grunewald K, Miller RJ, Osten P, Spear PG (2009) Infection of neurons and encephalitis after intracranial inoculation of herpes simplex virus requires the entry receptor nectin-1. Proc Natl Acad Sci USA 106: 17916–17920.

13. Bender SJ, Phillips JM, Scott EP, Weiss SR (2010) Murine coronavirus receptors are differentially expressed in the central nervous system and play virus strain-dependent roles in neuronal spread. J Virol 84: 11030–11044.

14. Havert MB, Schofield B, Griffin DE, Irani DN (2000) Activation of divergent neuronal cell death pathways in different target cell populations during neuroadapted Sindbis virus infection of mice. J Virol 74: 5352–5356.

15. Vernon PS, Griffin DE (2005) Characterization of an in vitro model of alphavirus infection of immature and mature neurons. J Virol 79: 3438–3447.

16. Rivas F, Diaz LA, Cardenas VM, Daza E, Bruzon L, et al. (1997) Epidemic Venezuelan equine encephalitis in La Guajira, Colombia, 1995. J Infect Dis 175: 828–832.

17. Haddow AD, Odoi A (2009) The incidence risk, clustering, and clinical presentation of La Crosse virus infections in the eastern United States, 2003-2007. PLoS ONE 4: e6145. doi: 10.1371/journal.pone.0006145.

18. Hayes EB, Komar N, Nasci RS, Montgomery SP, O’Leary DR, Campbell GL (2005) Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis 11: 1167–1173.

19. Conrady CD, Drevets DA, Carr DJ (2010) Herpes simplex type I (HSV-1) infection of the nervous system: is an immune response a good thing? J Neuroimmunol 220: 1–9.

20. Greene IP, Lee E-Y, Prow NA, Ngwang B, Griffin DE (2008) Protection from fatal viral encephalomyelitis: AMPA receptor antagonists have a direct effect on the inflammatory response to infection. Proc Natl Acad Sci USA 105: 3575–3580.

21. Tilleux S, Hermans E (2007) Neuroinflammation and regulation of glial glutamate uptake in neurological disorders. J Neurosci Res 85: 2059–2070.

22. Lafon M, Megret F, Meuth SG, Simon O, Velandia Romero ML, et al. (2008) Detrimental contribution of the immuno-inhibitor B7-H1 to rabies virus encephalitis. J Immunol 180: 7506–7515.

23. Lanteri MC, O’Brien KM, Purtha WE, Cameron MJ, Lund JM, et al. (2009) Tregs control the development of symptomatic West Nile virus infection in humans and mice. J Clin Invest 119: 3266–3277.

24. Burdeinick-Kerr R, Govindarajan D, Griffin DE (2009) Noncytolytic clearance of Sindbis virus infection from neurons by gamma interferon is dependent on Jak/STAT signaling. J Virol 83: 3429–3435.

25. Ubol S, Levine B, Lee S-H, Greenspan NS, Griffin DE (1995) Roles of immunoglobulin valency and the heavy-chain constant domain in antibody-mediated downregulation of Sindbis virus replication in persistently infected neurons. J Virol 69: 1990–1993.

26. Levine B, Hardwick JM, Trapp BD, Crawford TO, Bollinger RC, Griffin DE (1991) Antibody-mediated clearance of alphavirus infection from neurons. Science 254: 856–860.

27. Dorries R (2001) The role of T-cell-mediated mechanisms in virus infections of the nervous system. Curr Top Microbiol Immunol 253: 219–245.

28. Marten NW, Stohlman SA, Bergmann CC (2000) Role of viral persistence in retaining CD8(+) T cells within the central nervous system. J Virol 74: 7903–7910.

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Virology: Nature News Feature - XMRV could be an opportunistic infection affecting those whose immune systems are already dampened by CFS/ME

noreply@blogger.com (Ingrid J. Jones) — Mon, 14 Mar 2011 17:57:00 +0000

Researchers and public-health officials are scrambling to determine whether blood products could be spreading the virus XMRV (xenotropic murine leukaemia virus-related virus2), which has been linked to chronic fatigue syndrome (CFS) and prostate cancer.

Judy Mikovits, a viral immunologist at the Whittemore Peterson Institute for Neuro-Immune Disease (WPI) in Reno, Nevada, USA, says that she will not abandon the hypothesis that XMRV and related viruses cause CFS, despite a growing chorus of critics.

CFS, also known as myalgic encephalomyelitis (ME), affects an estimated 17 million people worldwide, but it is extremely difficult to diagnose. Many with the disorder are told that their symptoms — which include exhaustion, joint and muscle pain, cognitive issues, and heart and respiratory problems — are psychosomatic. "I had no idea there was that much bias against this disease," Mikovits says.

The stakes are high and many are taking the risks seriously. Several countries have barred people with chronic fatigue from donating blood in case the virus spreads. And the US government has launched a US$1.3-million study to investigate the link. Patients are already being tested for XMRV, and some are taking antiviral drugs on the assumption that the virus causes chronic fatigue by attacking their immune defences. Many say that such action is premature, but Mikovits is steadfast. "We're not changing our course," she says.

Full details below, in a copy of a news feature from Nature.com.

Note that even if a study confirms the link to chronic fatigue, it won't be able to determine whether the virus is the cause. XMRV could, for example, be an opportunistic infection affecting those whose immune systems are already dampened by chronic fatigue. Even Mikovits can only hypothesize as to how it might cause disease.

From Nature
Published online 14 March 2011
Virology: Fighting for a cause
By EWEN CALLAWAY (London)
Ref: Nature 471, 282-285 (2011) | doi:10.1038/471282a

When Judy Mikovits found links between chronic fatigue syndrome and a virus, the world took notice. Now, she's caught between the patients who believe her work and the researchers who don't.

On a sunny January afternoon in Santa Rosa, California, a small crowd waits patiently for Judy Mikovits to arrive. She is scheduled to deliver a talk on a mysterious virus called XMRV, which she believes underlies chronic fatigue syndrome. Although she's two hours late — held up by fog at San Francisco International Airport — not a single person has left. And when she arrives, they burst into applause.

To a rapt audience, she gives a chaotic and wide-ranging talk that explores viral sequences, cell-culture techniques and some of the criticisms that have been thrown at her since she published evidence1 of a link between XMRV and chronic fatigue in 2009. Afterwards, Mikovits is swarmed by attendees. A middle-aged woman who spent most of the talk in a motorized scooter stands up to snap pictures of her with a digital camera. Ann Cavanagh, who has chronic fatigue and has tested positive for XMRV, says that she came in part for information and in part to show her support for Mikovits. "I just wish there were a hundred of her," Cavanagh says.

The event was "surreal", says Mikovits, a viral immunologist at the Whittemore Peterson Institute for Neuro-Immune Disease (WPI) in Reno, Nevada. She is discomfited by the attention from patients, which at times borders on adulation. But her reception among scientists has been markedly cooler. Numerous follow-up studies have found no link between the virus and the disease; no group has published a replication of her findings; and some scientists argue that XMRV is an artefact of laboratory contamination. Now, even some of Mikovits's former collaborators are having second thoughts.

Mikovits has dug in, however, attacking her critics' methods and motives. She says that their distrust of her science stems from doubts about the legitimacy of chronic fatigue syndrome itself. Chronic fatigue, also known as myalgic encephalomyelitis, affects an estimated 17 million people worldwide, but it is extremely difficult to diagnose. Many with the disorder are told that their symptoms — which include exhaustion, joint and muscle pain, cognitive issues, and heart and respiratory problems — are psychosomatic. "I had no idea there was that much bias against this disease," Mikovits says.

The stakes are high and many are taking the risks seriously. Several countries have barred people with chronic fatigue from donating blood in case the virus spreads (see 'Something in the blood'). And the US government has launched a US$1.3-million study to investigate the link. Patients are already being tested for XMRV, and some are taking antiviral drugs on the assumption that the virus causes chronic fatigue by attacking their immune defences. Many say that such action is premature, but Mikovits is steadfast. "We're not changing our course," she says.

First findings

In October 2007, Mikovits attended a prostate-cancer meeting near Lake Tahoe, Nevada, where she met Robert Silverman, a virologist at the Cleveland Clinic in Ohio. Silverman co-discovered XMRV, which stands for xenotropic murine leukaemia virus-related virus2. While examining human prostate tumours, he and his collaborators found genetic sequences that resemble retroviruses found in the mouse genome. Like all retroviruses, XMRV rewrites its RNA genome into DNA on infection, then slips the DNA into the genomes of host cells. Ancient remnants of such viruses litter animal genomes. But the only active retroviruses conclusively linked to human disease are HTLV-1, which causes leukaemia, and HIV.

At the meeting, Silverman was presenting research linking XMRV to deficiencies in a virus-defence pathway. Mikovits recalled that the same pathway was weakened in some patients with chronic fatigue. She wondered whether the prostate-tumour virus could also be behind chronic fatigue. After the meeting, Silverman sent Mikovits reagents to test for XMRV.

The idea excited Mikovits, but she had other priorities. After stints in industry and at the US National Cancer Institute (NCI) in Maryland, she had recently joined the WPI to lead its research programme. The WPI was founded in 2006 by physician Daniel Peterson, an expert on chronic fatigue, and by Annette Whittemore, the wife of a well-connected Nevada businessman, whose daughter Andrea has had chronic fatigue for more than 20 years. The Whittemores spent $5 million establishing the WPI, and several million more to support Mikovits's research, which has attracted few other grants.

At the WPI, Mikovits established a sample collection from Peterson's patients and began screening it for signs of an infection. A litany of pathogens has been linked to chronic fatigue over the years, including Epstein-Barr virus, Borna disease virus, human herpes virus 6 and HTLV-2. None panned out. Still, the disorder bears some hallmarks of an infection. Many patients report acute illness before chronic symptoms appear, and their bodies often show signs of an immune system at war. The disease can also crop up in apparent outbreaks, including one characterized by Peterson near Lake Tahoe in the 1980s.

Just before Christmas 2008, Mikovits turned her attention to Silverman's reagents. She and her postdoc, Vincent Lombardi, known as Vinny, asked a graduate student to test for XMRV DNA in white blood cells from some of the most seriously ill people being studied at the WPI.

The first try turned up just two positives out of 20. But by tweaking the conditions of the test, Mikovits says her team found XMRV in all 20. "Vinny and I looked at each other and said, 'Well, that's interesting'," she says. They spent the next few weeks convincing themselves that they were onto something, and soon conscripted Silverman and Mikovits's former mentor at the NCI, Frank Ruscetti, to help prove that XMRV infection was behind chronic fatigue.

"We really retooled our entire programme and did nothing but focus on that," she says. They kept the effort under wraps, dubbing it 'Project X'. Even Peterson and the Whittemores weren't clued in. Mikovits says that the secrecy was necessary because her team also found XMRV in the blood of some healthy people, raising concerns about blood products. She hoped to build an airtight case because she worried that sceptical public-health officials would undermine her work.

In May 2009, the team submitted a paper to Science reporting the identification of XMRV genetic material in two-thirds of the 101 patients with chronic fatigue they had tested and in 3.7% of 218 healthy people. They also included data suggesting that infected white blood cells could pass the virus on to uninfected cells.

“They call me every single day. I spend so much time trying to understand the patients, to understand this disease.”
Reviewers wanted more evidence: a clear electron micrograph of virus-infected cells, proof that patients mounted an immune response to the virus, an evolutionary tree showing XMRV's relationship to other viruses and the locations where viral DNA was integrating into patient genomes. Mikovits's team went to work. "None of us took any time off, not even a weekend," she says. They resubmitted the paper in early July with everything the reviewers had asked for, except the DNA integration sites, which many scientists consider a gold standard in proving a retroviral infection.

Later that month, NCI officials who had learned about the work invited Mikovits to give a talk at a closed-door meeting with other XMRV researchers and government scientists. "When I finished speaking you could've heard a pin drop," she says. Mikovits says she thinks at least one of her manuscript's reviewers was at the meeting, because soon after, she got a call from a Science editor. Their paper had been accepted.

Jonathan Stoye, a retrovirologist at the MRC National Institute for Medical Research in London, wrote a commentary about the paper for Science3. He had never heard of Mikovits, but Frank Ruscetti's name on the paper gave him confidence, he says, and "if it were true, it was clearly very important". Stoye's co-author John Coffin, a retrovirologist at Tufts University in Boston, Massachusetts, says he was satisfied with the data and thought it was time to "let the field and public chew on them".

The BBC, US National Public Radio, The New York Times, The Wall Street Journal and dozens of other news outlets covered the research. "Prostate cancer pathogen may be behind the disease once dubbed 'yuppie flu'," Nature announced on its news website the day the paper came out. Phoenix Rising, a forum for patients with chronic fatigue that has become a hub for all things XMRV, called the work a "game changer", and patients flocked to learn more about a virus that they hoped would explain their condition. But others, including Britain's leading chronic fatigue patient group, urged caution until more research buttressed the link.

The first negative findings started to arrive in January 2010 — failing to find XMRV in 186 people with chronic fatigue from the United Kingdom4. A month later, a team including Stoye published a paper5 showing no evidence of XMRV in more than 500 blood samples from patients with chronic fatigue and healthy people. One day later, the British Medical Journal accepted a paper reporting more negative results in Dutch patients6. Studies began piling up so fast that Coffin made a scorecard to show at talks. "I've lost count now," he says.

Mikovits says that the discrepancies can be explained by differences in the geographical distribution of XMRV or in the methods used.

The most common way to detect XMRV is PCR, or polymerase chain reaction, which amplifies viral DNA sequences to a level at which they can be identified. Mikovits and her team used this method to detect XMRV in some of their patients, but she contends that the most sensitive way to detect the virus is to culture patients' blood cells with a cell line in which the virus replicates more quickly. This should create more copies of the virus, making it easier to detect with PCR and other techniques. She says that none of the negative studies applied this method exactly, a fact that annoys her. "Nobody's tried to rep-li-cate it," she says, sounding out each syllable for emphasis.

In summer 2010, some evidence emerged in Mikovits's corner. Harvey Alter, a hepatitis expert at the NIH's Clinical Center, and his team identified viruses similar to XMRV in 32 of 37 people with chronic fatigue and in 3 of 44 healthy people. They were preparing to publish their results in the Proceedings of the National Academy of Sciences. But scientists at the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, were about to publish a negative report. The authors delayed publication of both papers7,8 for several weeks to assess discrepancies. The move agitated Mikovits as well as the chronic-fatigue community, who suspected that important data were being suppressed.

When Alter's work came out in late August7, Mikovits was ecstatic, and the WPI released a YouTube video of her touting it. For other researchers, however, the new paper had shortcomings. The viral sequences from Alter's paper differed from XMRV, says Greg Towers, a retrovirologist at University College London. "He doesn't get variation, he gets a totally different virus." Towers says that mouse DNA, which is chock-full of virus sequences like those Alter's team found, probably contaminated their samples, which were collected in the 1990s. But Alter says that his team found no contamination from mouse DNA and recovered the same viral sequences from the same patients sampled a decade later.

Contamination became a dirty word for Mikovits. Just before Christmas 2010, Retrovirology published four papers9,10,11,12 that highlighted laboratory contamination as a possible explanation for her findings. One showed, for example, that mouse DNA contaminates an enzyme from a commercial kit commonly used for PCR. Coffin, an author on two of the Retrovirology papers, urges caution against over-extrapolating. These papers do not say that contamination explains Mikovits's results, he says, just that extreme care is required to avoid it.

Towers and his colleague Paul Kellam, a virologist at the Wellcome Trust Sanger Institute near Cambridge, UK, are less charitable, however. Their study12 showed that the XMRV sequences that Mikovits and Silverman had extracted from patients lacked the diversity expected of a retrovirus that accumulates mutations as it passes between patients. "This doesn't look like an onwardly transmittable infectious virus," says Kellam. A press release for the paper issued by the Sanger Institute put it more bluntly: "Chronic fatigue syndrome is not caused by XMRV."

Mikovits is riled when the topic turns to Towers's paper over dinner one night in Reno — "Christmas garbage", she calls it. Contamination cannot explain why her team can reproduce its results both in her lab in Reno and at Ruscetti's at the NCI, she says. Her team checks for contamination in reagents and in the cells it grows the patients' samples with. She says that her team has also collected viral sequences that will address Towers's and Kellam's criticism but that it hasn't yet been able to publish them. Meanwhile, an unpublished study of patients in Britain with chronic fatigue bears out the link to XMRV, she says. "I haven't for one second seen a piece of data that convinced me they're not infected."

Jay Levy, a virologist at the Univer sity of California, San Francisco, has a window in his closet-sized office that looks out into the laboratory where, in the 1980s, he became one of the first scientists to isolate HIV. After his discovery was scooped by other researchers, Levy turned his attention to chronic fatigue and started a long but fruitless search for an infectious cause.

Now, Levy is putting the finishing touches on what could be the most thorough response yet to Mikovits's Science paper, adopting the same cell-culture techniques to detect the virus and using samples from the same patients. He's done this with the help of Daniel Peterson, who left the WPI in 2010 for what Peterson says are "personal reasons". Peterson has questioned the institute's singular pursuit of XMRV, a research direction that was pursued without his consultation.

Mikovits says that she kept the XMRV work secret from Peterson over fears he would tell his patients, and left his name off the original Science manuscript until a reviewer questioned the omission. When asked whether that episode contributed to his departure, he says, "I was surprised at the secrecy and lack of collaboration." As for his motivation to team up with Levy: "I'm just trying to get to the truth. It's my only motive, because this is such a deserving group of patients who need to know what's going on."

Others, too, are rallying for a definitive answer. Ian Lipkin, a microbial epidemiologist at Columbia University in New York, has a reputation for getting to the bottom of mysterious disease–pathogen links. His team debunked the association between Borna disease virus and chronic fatigue, for example. Now he is spearheading the $1.3-million effort funded by the US government. He is leaving the testing to three labs: Mikovits's at the WPI, Alter's at the NIH and the CDC. Each will receive coded samples of white blood cells and plasma from 150 patients with chronic fatigue and from 150 healthy controls. The labs will test for XMRV using their method of choice. Lipkin will crunch the data and unblind the samples.

But even if a study confirms the link to chronic fatigue, it won't be able to determine whether the virus is the cause. XMRV could, for example, be an opportunistic infection affecting those whose immune systems are already dampened by chronic fatigue. Even Mikovits can only hypothesize as to how it might cause disease.

The virus might not even exist as a natural infection. At a retrovirus conference this month in Boston, Massachusetts, Coffin and his colleague Vinay Pathak at the NCI in Frederick, Maryland, presented data showing that XMRV emerged in the 1990s, during the development of a prostate-tumour cell line called 22Rv1. Developing the line involved implanting a prostate-tumour sample into mice, retrieving cells that might divide indefinitely and repeating the process. But looking back at DNA samples taken throughout the cell-line's development showed that human cells became infected only after passing through several different mice. Importantly, XMRV's sequence seems to have come from two different mouse strains. "They just sort of snapped together like two puzzle pieces," says Coffin, an event extremely unlikely to have happened twice.

XMRV sequences retrieved from patients with prostate cancer and chronic fatigue — including some who have had chronic fatigue since the mid-1980s — are nearly identical to the virus from 22Rv1 cells. The implication, says Coffin, is that this virus, born in a laboratory, has probably been infecting samples for more than a decade, but not people. "Although people on the blogs aren't going to believe me, I'm afraid this is by far the most reasonable explanation for how XMRV came to be," says Coffin, who hoped that the association with chronic fatigue would pan out and still thinks some pathogen other than XMRV could explain the disease.

Silverman, who no longer works with Mikovits, says that he wasn't using 22Rv1 cells when XMRV was discovered. Nonetheless, the work has rattled his confidence in XMRV's link to both prostate cancer and chronic fatigue.

Mikovits, however, is undeterred. The WPI owns a company that charges patients up to $549 to be tested for XMRV, and Mikovits believes that patients who test positive should consult their doctors about getting antiretroviral drugs normally prescribed to those with HIV. Levy and others worry that she is overreaching. "That's scary for me. These antiretroviral drugs are not just like taking an aspirin," he says. Mikovits argues that they might be some patients' only hope. "The people who we know they're infected should have a right to get therapy," she says, "They have nothing. They have no other choice."

Context and debate

Back in her Reno laboratory two days after the talk in Santa Rosa, Mikovits examines a stack of small plastic flasks under a microscope. Some contain patient cells that she hopes will turn into cell lines and churn out XMRV. "On Wednesdays I get to take care of my cells, and that's where I'm the happiest," she says.

She has just come off the phone from a sobbing patient infected with XMRV whose symptoms had worsened. "They call me every single day," Mikovits says. "I don't do science any more. I spend so much time trying to understand the patients, to understand this disease. People have moved to Reno to be here," she says. They've left gifts: stuffed animals, and stacks of bumper stickers that say "Today's Discoveries, Tomorrow's Cures" and, more boldly, "It's the virus XMRV".

Mikovits clearly shares in the frustration of those with chronic fatigue who have been marginalized over the years and told that their disease is not real. She says that this disbelief in the disorder drives the criticism of her work. Kellam and the others say that this isn't true. They don't deny the existence of the syndrome or even the possibility of an infectious origin. "What we're trying to understand is the aetiology," Kellam says. "It's a scientific debate."

Mikovits says that she's analysed all the papers critical of her work and found flaws in each of them. Nevertheless, she's quick to endorse findings that support her work. She claims that Coffin and Pathak's study, for example, "says nothing about human infection". Yet new work presented at a different meeting that found XMRV using next-generation DNA sequencing offers "no doubt it's not contamination — that the whole story's real", she says.

Despite the growing choir of sceptics, Mikovits says that she has simply seen too many data implicating XMRV and other related viruses in chronic fatigue to change her mind. For her supporters, that steadfastness offers legitimacy and hope. "The scientists are moving forward," she announced at her talk in Santa Rosa, "and I think the politics will go away shortly." The crowd responded with vigorous applause.

Ewen Callaway writes for Nature from London.

References
Lombardi, V. C. et al. Science 326, 585-589 (2009).
Urisman, A. et al. PLoS Pathog. 2, e25 (2006).
Coffin, J. M. & Stoye, J. P. Science 326, 530-531 (2009).
Erlwein, O. et al. PLoS ONE 5, e8519 (2010).
Groom, H. C. et al. Retrovirology 7, 10 (2010).
Van Kuppeveld, F. J. et al. Br. Med. J. 340, c1018 (2010).
Lo, S. C. et al. Proc. Natl Acad. Sci. USA 107, 15874-15879 (2010).
Switzer, W. M. et al. Retrovirology 7, 57 (2010).
Robinson, M. J. et al. Retrovirology 7, 108 (2010).
Oakes, B. et al. Retrovirology 7, 109 (2010).
Sato, E. , Furuta, R. A. & Miyazawa, T. Retrovirology 7, 110 (2010).
Hué, S. et al. Retrovirology 7, 111 (2010).

[Ends]

Ewen Callaway, London
Ewen Callaway joined Nature in August 2010, after 2 years at New Scientist as Boston-based biomedical reporter. He attended the science writing program at the University of California, Santa Cruz and earned a masters degree in microbiology at the University of Washington. He spends his free time learning to bicycle on the left side of the road.
- - -

'Something in the blood'
From the article:
Virology: Fighting for a cause*

Researchers and public-health officials are scrambling to determine whether blood products could be spreading the virus XMRV, which has been linked to chronic fatigue syndrome (CFS) and prostate cancer.

2009

October Judy Mikovits publishes a paper showing XMRV in two-thirds of patients with CFS and in 4% of healthy individuals1.

December The US Department of Health and Human Services establishes a working group and the AABB (formerly the American Association of Blood Banks) organizes a task force to assess the prevalence of XMRV in blood products and the risk of its transmission.

2010

April Australia, Canada and New Zealand ban people with a history of CFS from donating blood.

June The task force recommends that patients with CFS be discouraged from donating blood in the United States.

November Britain bans patients with CFS from donating blood, officially to protect them from a decline in health.

December The working group reports discordant results of a pilot study on XMRV blood contamination, but recommends banning patients with CFS from donating blood.

The American Red Cross bans blood donations from people with a history of CFS.

2011

March At a retrovirology meeting in Boston, Massachusetts, researchers present data suggesting that XMRV is a laboratory artefact and not a human pathogen.

*Download a PDF of the article
Virology: Fighting for a cause*

Chronic Neuroimmune Diseases - CFS: A polio by another name

noreply@blogger.com (Ingrid J. Jones) — Tue, 04 Jan 2011 22:14:00 +0000

From The New York Times
January 3, 2011
Exhausted by Illness, and Doubts
By DAVID TULLER

Chronic fatigue syndrome causes a host of debilitating symptoms: profound exhaustion, disordered sleep, muscle and joint pain and severe cognitive problems, among others. But what causes the syndrome itself?

Since the first cases in the United States were identified in the 1980s, scientists have been divided over that question. Some have suspected that one or more viral infections are likely to play a central role.

But many other researchers — not to mention relatives, friends, employers, doctors and insurers of the million or more Americans estimated to suffer from the illness — have dismissed it as stress-related, psychosomatic or simply imaginary.

Now recent back-to-back announcements have highlighted both the volatility of the issue and the ambiguity of the science, and have alternately heartened and dismayed patients.

On Dec. 14, an advisory panel suggested that the Food and Drug Administration ban blood donations by people with a history of C.F.S., as the illness is often called. The goal was to prevent the possible spread of viruses that two high-profile studies had linked to the condition.

But then, on Dec. 20, the journal Retrovirology published four papers suggesting that key findings in those studies could have resulted from laboratory contamination.

The F.D.A. is not required to accept the opinion of its advisory panel. Yet patients still hailed the recommendation as a sign that their illness was being taken seriously.

“When an F.D.A. panel suggests that patients with C.F.S. not donate blood, that’s going to impact the way doctors think about it,” said Mary Schweitzer, a former history professor at Villanova, who has frequently written about living with the illness. Dr. Schweitzer said she has been unable to work for 16 years because of the syndrome, which was diagnosed after she suffered from a series of flulike illnesses.

The studies that concerned the F.D.A. had reported that people with the syndrome, which is also called myalgic encephalomyelitis or myalgic encephalopathy in Europe, showed higher rates of infection with the virus XMRV or others from the same category, known as MLV-related viruses. (These viruses are all relatives of mouse leukemia viruses, some of which can infect species other than mice; their role in human disease, if any, remains poorly understood.)

But several other research teams in the last year have found no connection between chronic fatigue syndrome and these viruses, although none tried to replicate the exact methods used by researchers who reported an association.

The new papers in Retrovirology reported that contamination of tissue samples or other laboratory items with mouse DNA or viral genetic material could lead to false positive results for XMRV, and by extension other MLV-related viruses, specifically when using polymerase chain reaction technology. The technique rapidly produces millions of copies of genetic segments, so even minute traces of genetic contamination can skew results.

“Our conclusion is quite simple: XMRV is not the cause of chronic fatigue syndrome,” said the senior author of one of the studies, Greg Towers, a professor of virology at University College London, in a statement released by Wellcome Trust Sanger Institute, the British research center that co-sponsored it.

Other scientists and advocates for patients have sharply criticized such certainty as unwarranted, noting that the Retrovirology papers themselves expressed their findings in more cautious terms. The critics agree that contamination can be a serious issue when using polymerase chain reaction technology. But the new papers, said Eric Gordon, a doctor in Santa Rosa, Calif., who treats many patients with the illness, do not evaluate other strategies besides P.C.R., as the technique is known, for detecting the MLV-related viruses, like testing for an immune response and culturing the viruses in cell lines.

“The articles make the point that P.C.R. doesn’t work that well for these viruses, and then they act like that disproves the whole idea,” said Dr. Gordon.

XMRV was first identified in 2006 and has been detected in prostate cancer patients in some studies. It was linked to chronic fatigue syndrome in October 2009 in a paper in the journal Science by researchers from the Whittemore Peterson Institute for Neuro-Immune Disease at the University of Nevada, Reno, the National Cancer Institute and the Cleveland Clinic.

The researchers relied on P.C.R. technology to show that about two-thirds of patients but less than 4 percent of control subjects harbored XMRV. Using other technologies, however, they also documented an antibody response in some chronic fatigue syndrome patients, and reported that XMRV in human blood could infect other human cell lines.

In a statement responding to the new papers in Retrovirology, Judy A. Mikovits, director of research at Whittemore Peterson and the senior author of the Science study, said her team took extensive steps to rule out P.C.R. contamination and also focused on other approaches to finding XMRV. “Nothing that has been published to date refutes our data,” she said.

Even some specialists stumbled over the meaning of the new findings. Vincent Racaniello, a professor of microbiology at Columbia not involved in the research, apologized on his Virology Blog for having stated that it was likely to spell “the beginning of the end” for the proposed connection between the viruses and chronic fatigue syndrome.

After reviewing the issue more thoroughly, he wrote, he realized that the new studies “show that identification of XMRV can be fraught with contamination problems, but they do not imply that previously published studies are compromised.” He added, “If I had difficulties interpreting these papers, how would nonscientists fare?”

Federal agencies have come down on different sides of the issue. In a paper published in The Proceedings of the National Academy of Sciences in August, researchers from the National Institutes of Health and the F.D.A. found a link between the fatigue syndrome and MLV-related viruses (although not specifically XMRV). In contrast, a study from the Centers for Disease Control and Prevention was among those not reporting a link.

Federal health officials have organized two research efforts to resolve the inconsistencies, determine whether XMRV and MLV-related viruses are possible human pathogens, and identify reliable ways to detect them. Patients hope the increased attention will quickly lead to research on treatments, including clinical trials of H.I.V. drugs, some of which have been shown in lab studies to inhibit the replication of XMRV.

The unsettled situation has created a quandary for patients with chronic fatigue syndrome and the doctors who treat them. Some patients are seeking to be treated with H.I.V. drugs, which doctors can legally prescribe even though the F.D.A. has not approved them for that purpose.

Many doctors and researchers say it is too early to prescribe the drugs for chronic fatigue because of possible side effects, like bone marrow suppression, gastrointestinal problems and liver or kidney dysfunction, among others. But Michael Allen, a writer and a former psychologist in San Francisco who has been disabled for more than 15 years, said he wouldn’t hesitate to try the medications if he found out he was positive for an MLV-related virus.

“It feels patronizing when the medical establishment says the side effects are too risky and we should keep waiting,” he said. “What that says to me is they have no idea whatsoever how sick people like me have been with this disease.”
[End of copy]

- - -

NOTES TO SELF

Enterovirus: Coxsackie B virus
Symptoms of infection with viruses in the Coxsackie B grouping include fever, headache, sore throat, gastrointestinal distress, as well as chest and muscle pain. [...] As of 2008, there is no well-accepted treatment for the Coxsackie B group of viruses.

Coxsackie B viruses can cause mild signs and symptoms, similar to a "cold", but these viruses also can lead to more serious diseases, including myocarditis (inflammation of the heart); pericarditis (inflammation of the sac lining the heart); meningitis (inflammation of the membranes that line the brain and spinal cord); and pancreatitis (inflammation of the pancreas).
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Coxsackie_B_virus
- - -

Poliomyelitis
The term poliomyelitis is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or non-paralytic.[9] In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illness.[4]
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Poliomyelitis
- - -

Cortisol
Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor.[32] Cortisol also has a negative feedback effect on interleukin-1.[33] IL-1 must be especially useful in combating some diseases; however, endotoxin bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels via forcing secretion of CRH hormone, thus antagonizing IL-1 in this case.
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Cortisol
- - -

Chronic Neuroimmune Diseases
Information on CFS, FM, MCS, Lyme Disease, Thyroid, and more...
Last updated December 18, 2009
Chronic Fatigue Syndrome
A polio by another name
Read more at:
http://www.anapsid.org/cnd/diffdx/polio1.html
- - -

Ampligen
Ampligen was first synthesized in the 1970s and has been proposed and tested as a treatment for illnesses including chronic fatigue syndrome (CFS) and acquired immunodeficiency syndrome (AIDS).
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Ampligen
- - -

Co-codamol
Co-codamol (BAN) is a non-proprietary name used to denote a compound analgesic, a combination of codeine phosphate and paracetamol (acetaminophen). Co-codamol tablets are used for the relief of mild to severe pain.
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Co-codamol
- - -

Nabilone
Nabilone is a synthetic cannabinoid with therapeutic use as an antiemetic and as an adjunct analgesic for neuropathic pain. It is a synthetic cannabinoid, which mimics the main ingredient of cannabis (THC). Chemically, nabilone is similar to the active ingredient found in naturally occurring Cannabis sativa L. [1]
In Canada, the United States, the United Kingdom and Mexico, nabilone is marketed as Cesamet. It was approved in 1985 by the U.S. Food and Drug Administration (FDA) for treatment of chemotherapy-induced nausea and vomiting that has not responded to conventional antiemetics. Though it was approved by the FDA in 1985, the drug only began marketing in the United States in 2006. It is also approved for use in treatment of anorexia and weight loss in patients with AIDS.
Although it doesn't have the official indication (except in Mexico), nabilone is widely used as an adjunct therapy for chronic pain management. Numerous trials and case studies have demonstrated various benefits for condition such as fibromyalgia[2] and multiple sclerosis.[3]
Read more at Wikipedia:
http://en.wikipedia.org/wiki/Nabilone
- - -

Dorset woman with severe ME 'left to rot by the NHS'

noreply@blogger.com (Ingrid J. Jones) — Thu, 25 Nov 2010 17:58:00 +0000

Libby Meyers was first diagnosed with ME in 2000 and by 2002 she was bed-bound. About 150,000 people in the UK have ME and of them about 3% have symptoms classed as severe.

Source: www.bbc.co.uk
Dorset woman with severe ME 'left to rot by the NHS'
Date: Thursday, 25 November 2010 at 06:00

CFS: XMRV could be a 'rumour virus' - Where have the epidemiologists been all this time? I am an emergency doctor and this is an emergency!

noreply@blogger.com (Ingrid J. Jones) — Sat, 18 Sep 2010 16:49:00 +0000

My written testimony to the CFSAC
From X Rx blog - Friday, 17 September 2010:

Testimony of Jamie Deckoff-Jones MD
CFSAC
September 17, 2010

To whom it may concern:

I am a 56 year old emergency physician. I have been diagnosed with CFS, chronic Lyme Disease and atypical MS. My 20 year old daughter has been diagnosed with CFS and chronic Lyme Disease. I have been ill for 16 years and disabled for 6. My daughter has been ill for 7 years and disabled for 4. In the last few years, I have almost died twice and my daughter has been hospitalized for cerebral vasculitis. My husband has been ill for 7 years and is functional. My 15 year old son is clinically healthy.

In October of last year, I read the Mikovits paper in Science. It was immediately apparent to me that our illness was of retroviral origin. In February, my daughter and I tested positive for XMRV by culture. We were both almost housebound at that time. With the help of a compassionate family doctor and the guidance of an experienced AIDS doctor, we started the three antiretroviral drugs that tested in vitro against XMRV in the Singh study. Six months later, my daughter has started community college and I am planning a return to part-time practice. As always with clinical medicine, there are confounders, but I do not think it possible that we have not been helped by antiretroviral therapy.

Because the patients have no help, I started a blog to share our experiences with treatment and my clinical ideas. The response has been enormous. My email is filled with stories of unbelievable pain, neglect and abuse. The wasted lives and wasted talent are a national disaster. Instead of contributing, a staggering number of people are unable or almost unable to care for themselves.

Since CFS patients don’t die from their disease for a very long time, there is a tendency to feel that there is no hurry. Good science takes time after all. But it is a progressive disease. There are a staggering number of patients who are too sick to wait. They need compassionate care. They’ve been denied basic care, even common decency, for decades. It’s been a year since the association between XMRV and CFS was elucidated. Scientists say causation has not yet been demonstrated. I say it should be a clinical assumption at this point. As a physician, it’s obvious from the stories and family histories of the patients contacting me. Where have the epidemiologists been all this time? I am an emergency doctor and this is an emergency!

To me, it’s a miracle that existing safe drugs may be effective. It is a travesty that clinical trials have not yet begun. It brings shame on the medical profession that doctors are unable to connect the dots. If there was a hurricane or an earthquake, everybody would be rushing to help. Even if all resources are immediately mobilized, many will be lost. The patients have very advanced disease. It is beyond a disaster.

New babies are being born with it every day. Is it possible that AZT in pregnancy will prevent it, as it does HIV? Why is nobody trying to find out?

The WPI has single-handedly made things happen for patients. Why are they not funded? They are a tiny non-profit. They have handed the world the answer on a silver platter. Is our government ever going to step up to the plate?

Sincerely,
Jamie Deckoff-Jones MD
Santa Fe, NM

- - -

Wessely's co-author: XMRV could be a 'rumour virus'

Hat tip: http://chronicfatiguesyndrome.co.nz

Abundant Evidence ME/CFS is Neurological - Harvard's Dr. Komaroff

noreply@blogger.com (Ingrid J. Jones) — Thu, 10 Jun 2010 14:22:00 +0000

Abundant Evidence ME/CFS is Neurological - Harvard's Dr. Komaroff
Report from ProHealth.com - Wednesday, 09 June 2010:

On April 24, the Massachusetts CFIDS/ME & FM Association hosted a presentation on “The Latest Research on CFS” by Dr. Anthony L Komaroff, MD. Dr. Komaroff , a professor of medicine at Harvard Medical School and Editor in Chief of Harvard Health Publications, has treated hundreds of ME/CFS patients over the past 25 years.

Excellent Videos Available Free Online (Full Text Scripts Promised Soon)
Now, with Dr. Komaroff’s permission, the Mass. CFIDS Assoc. has made Dr. Komaroff’s lecture and extensive audience Q&A available on their website (www.masscfids.org/news-a-events. The videos take time to download, but the visual and sound quality are first-rate.

Owing to Dr. Komaroff’s unimpeachable reputation and status in the medical community, patients and advocates may wish to share links to these highly organized and informative videos with their own healthcare providers.

Easy to Follow
You can view each session from beginning to end - or click on any of the numbered topics listed down the left side of the screen, to view only those parts. (For a preview of the topics & questions covered, see our listings, below. If you’re like us, you may start with ‘dessert’ – the Q&A.)

Notable Quotes
In answer to question # 21 in the Q&A session – “Would you classify CFS as a neurological disease?” Dr. Komaroff stated:

"I would certainly say, as I have said today, that there is now abundant evidence of measurable abnormalities in the central nervous system and the autonomic nervous system in people with this illness. So that makes it neurological. That's why I think it makes sense, as Dr. Gurwitz said, to call it Myalgic Ecephalomyelitis or Encephalopathy, because I think those two words adequately classify or describe an underlying biology that tests have shown to be the case."

In answer to question # 26 - “With respect to the study on the presence of metabolites after exercise, how do patients with depression compare to CFS patients?” Dr. Komaroff stated:

“As a doctor who has taken care of patients with major depression for many years I can’t recall a single instance of someone with major depression saying, ‘The strangest thing has been happening to me, doctor, whenever I do anything, any physical exertion, the next day I feel completely beat up.’ I have never heard that from any patient with any illness other than chronic fatigue syndrome.”

* * * *
VIDEO: Dr. Komaroff’s Pre-prepared Q&A – 22 Minutes
Link to video: www.masscfids.org/videofiles/Questions/Questions.html

Preview of questions:
1. Intro – (Dr. Komaroff mentions his responses are based on 25 years’ experience managing hundreds of ME/CFS patients)

2. Would having patients write their stories in detail help the process of discovery of this illness and how to treat it?

3. What is the trajectory or course of the illness in people, in your experience?

4. What is the best way to transition children from pediatric doctors to adult doctors?

5. Have you treated patients with anti-virals with any success?

6. If a CFS patient had persistent lab evidence of Epstein-Barr virus reactivation, would you treat it?

7. What are the objective biological markers that distinguish CFS from MS or Lyme disease?

8. Is there a link between CFS and chemical sensitivities?

9. How does Fibromyalgia fit into CFS?

10. Is there any treatment that helps?

11. How can I best determine if I have an HHV6 infection?

12. What do you think about the proposal to classify CFS in the Somatiform Disorder section of the new Diagnostic Statistical Manual?

13. Are new cutting edge state of the art treatment approaches like stem cell therapy likely to offer any answer for CFS?

14. Can you give us an update on Ampligen?

15. Are there new clinical protocols that MDs should follow in treating someone with CFS and should a patient go to an infectious disease doctor?

16. Can the mitochondrial link be exploited by mitochondrial manipulation?

17. Can CFS be triggered by exposure to a dry cleaning product and is this a common reaction?

18. What are some other examples of illnesses caused by multiple viruses that wind up with the same symptoms as CFS?

19. Why does the CDC ignore or deny abnormalities and say no tests in CFS?

20. Of the 11% of patients in the Australian study who developed CFS, was there a difference between those who had a slow onset versus a sudden onset?

21. Would you classify CFS as a neurological disease?

22. What have been the most effective treatments to manage the symptoms and are they all palliative?

23. Are there any current or upcoming XMRV studies in the Boston area?

24. What do you think of treatment with low-dose Naltrexone?

25. Is there a list of local providers who specialize in CFS?

26. With respect to the study on the presence of metabolites after exercise, how do patients with depression compare to CFS patients?

27. Do you think there is a connection between CFS & Mercury? Autism? Food sensitivities?

* * * *
VIDEO: Dr. Komaroff’s Presentation on “The Latest Research on CFS” – 1 hour
Link to video - www.masscfids.org/videofiles/Komaroff/Komaroff.html

Preview of topics:
1. Intro

2. CDC case definition of Chronic Fatigue Syndrome

3. Chronic Fatigue Syndrome research

4. Severity of CFS

5. SF36 Health Status Subscale Scores

6. Lost productivity from CFS: CDC analysis

7. Is CFS real? (Biological markers? Understand how symptoms are caused?)

8. How is the body affected by CFS?

9. The brain in CFS

10. Evidence of brain involvement in CFS

11. Protemic markers in spinal fluid

12. Lactate in spinal fluid in CFS

13. EEG: Spectral coherence studies

14. Molecular sensors of fatigue & pain

15. Fatigue & pain sensing molecules

16. The immune system in CFS

17. Immunological abnormalities in CFS

18. Energy metabolism in CFS

19. The energy metabolism hypothesis

20. Genetic component to CFS

21. Gene expression studies in CFS

22. Infections in CFS

23. Infection: Temporary vs. permanent

24. Infections & syndromes: More than one microbe

25. Viruses and CFS

26. Infectious agents linked to CFS

27. Documentation of post-infectious CFS

28. Enteroviral infection in CFS

29. Enterovirus VP1 Ag in Gastric Antrum

30. Neurological findings in patients with CFS

31. HHV-6 and the brain

32. Active HHV6 infection in CFS: Study results

33. XMRV (Retrovirus) in CFS (slide 1)

34. XMRV (Retrovirus) in CFS (slide 2)

35. XMRV (Retrovirus) in CFS (slide 3)

36. What if XMRV is associated with CFS

37. Viruses and CFS – my current view

38. Concluding thoughts

April 12, 2010: Whittemore Peterson Publicly Challenges UK Researchers to Collaborate on XMRV & ME/CFS Research

noreply@blogger.com (Ingrid J. Jones) — Tue, 13 Apr 2010 18:12:00 +0000

From ProHealth.com - Tuesday, 13 April 2010:

April 12: Whittemore Peterson Publicly Challenges UK Researchers to Collaborate on XMRV & ME/CFS Research

Annette Whittemore, Founder & CEO of the Whittemore-Peterson Institute, issued the following public letter to ME/CFS researchers in the UK – essentially challenging them to collaborate in studies of the ME/CFS and the XMRV retrovirus, so as to move the science forward.

The open letter is addressed to Myra McClure, co-author with Simon Wessely of the editorial “Chronic fatigue syndrome and human retrovirus XMRV - Three studies now refute the original study reporting the link” published Feb 25, 2020 in the BMJ (British Medical Journal). It states, in part, “In January 2010, our own group found no evidence of XMRV in a well characterised cohort of 186 patients with chronic fatigue syndrome in the United Kingdom.” Dr. McClure is professor of retrovirology at Imperial College London. Dr. Wessely is professor of psychological medicine at Kings College, London.

The following letter may be reproduced by permission of the WPI.

Whittemore Peterson
Institute for Neuro-Immune Disease
Annette.Whittemore@WPInstitute.org

April 12, 2010

Dear Dr. McClure:

On behalf of the Whittemore Peterson Institute in Reno, Nevada (“WPI”), I am writing you today to ensure that there is direct communication between WPI and your research team.

You may share this letter with others that you deem appropriate, and I will do the same by sharing this letter with other interested parties in both the United States and the United Kingdom.

On January 6, 2010, you reported in PloS One that you failed to detect xenotropic murine leukemia virus-related virus (“XMRV”) in ME/CFS patient samples.

In that publication you reported the following conclusion, “based on our molecular data, we do not share the conviction that XMRV may be a contributory factor in the pathogenesis of ME/CFS, at least in the U.K.”

You subsequently made the following statement in your commentary regarding the Netherlands study in the BMJ, “….van Kuppeveld and colleagues provide the additional information reported at a conference last year that the patients in question came from an outbreak of chronic fatigue syndrome at Incline Village on the northern border of Lake Tahoe in the mid-1980s.”

This statement about the origin of the 101 patient samples is untrue. The patients in the Science study were well defined in the paper as having CFS by the Fukuda and Canadian consensus definitions of ME/CFS.

More importantly the patient samples did not come from the “Lake Tahoe outbreak” as you assert, but rather from patients who had become ill while living in various parts of the United States.

We would also like to report that WPI researchers have previously detected XMRV in patient samples from both Dr. Kerr’s and Dr. van Kuppeveld’s cohorts prior to the completion of their own studies, as they requested.

We have email communication that confirms both doctors were aware of these findings before publishing their negative papers.

In addition, Dr. van Kuppeveld asked for and received reagents and a positive patient sample to determine if his testing procedures could in fact detect XMRV in a positive blood sample before he published his paper. We wonder why these materials were not used in his study which also failed to detect XMRV.

One might begin to suspect that the discrepancy between our findings of XMRV in our patient population and patients outside of the United States, from several separate laboratories, are in part due to technical aspects of the testing procedures.

To help identify the possible reasons for the discrepancies in detection of XMRV, WPI would like to send you known positive patient samples with controls, from the United States in an appropriate number, along with WPI reagents, so that we can help you determine whether your testing methodologies will accurately detect XMRV in a clinical sample of blood.

In addition, WPI would be willing to test a like number of samples from your patient cohort to see if our researchers can detect XMRV in those samples.

This critical exercise would help resolve the question of whether you are using all of the appropriate techniques necessary to detect XMRV in a patient’s sample.

If your tests are able to detect XMRV correctly in the known positives, then the debate can appropriately center on whether we can identify the differences in the patient cohorts which have been the subject of
various studies.

It is in this systematic manner that we all may help to move the science forward; instead of continuing to debate whether or not ME/CFS patients in Europe are infected with XMRV.

It is also important to note that our initial study was not intended to prove causality of ME/CFS, but to report a significant association between patients who had been diagnosed with ME/CFS and XMRV.

We believe that there exists compelling evidence to spur additional scientific review, especially in light of the fact that our team of researchers also discovered XMRV in the blood of 3.7% of our non contact controls.

I look forward to your timely reply.

Sincerely,
Annette Whittemore
Founder and CEO
Whittemore Peterson Institute

New Suspect In Gulf War Syndrome

noreply@blogger.com (Ingrid J. Jones) — Sat, 06 Mar 2010 18:31:00 +0000

Research from several labs on microglia in chronic pain has identified many steps in this neuro-immune signaling process that become disrupted and researchers have found specific drugs to restore the normal function of these pain circuits, thus ending the chronic pain. Most of this work is in laboratory animals but clinical studies are now under way.

New Suspect In Gulf War Syndrome
From The Huffington Post
By Dr. Douglas Fields,
Posted: March 3, 2010 02:25 PM

Washington, D.C.-- On February 26, 2010, the Veterans Affairs Department announced that it will re-examine the disability claims of thousands of Persian Gulf War veterans still suffering from the mysterious Gulf War illnesses two decades after the war ended. At a meeting of the Federal Advisory Committee on Gulf War Veteran's Illnesses held yesterday in Washington, D.C., scientists from around the country presented their latest research to committee members searching for clues to this mysterious illness. Early in the meeting a new culprit emerged -- "the other brain" -- the non-electric portion of the brain composed of brain cells called glia.

"This is one of the best explanations I've heard," commented distinguished neuroscientist Floyd Bloom, after a presentation by Dr. Linda Watkins of the University of Colorado speaking about her latest research showing that glial cells, called microglia, are the unsuspected agents in chronic pain and drug addiction. Previously neurons were thought to be the sole cause of chronic pain and morphine tolerance. However, the new insight into how these "immune cells" of the brain aggravate neurons after an injury by releasing substances that produce excruciating pain, a parallel with Gulf War Syndrome became apparent.

Gulf War syndrome is characterized by a collection of unexplained symptoms, many of them neurological, including chronic pain, chronic fatigue, depression, sleep disturbances, memory loss, as well as gastrointestinal and lung problems. A number of causes have been suspected, including exposure to low-level neurotoxins, including sarin gas, drugs taken to protect soldiers from biological and chemical warfare agents, pesticides used to treat tents and soldier's uniforms stationed in the desert, depleted uranium from munitions, and the toxic mixture of fumes released for a year after the war ended from oil fields set ablaze by the retreating Iraq soldiers. The toxic fumes blotted out the sun at midday for miles.

Many people suffer chronic pain after an injury. Unlike normal pain, chronic pain does not end after the injury heals; in fact it often gets worse. The latest research shows that chronic pain results from an interaction between the immune system and the brain. When we are sick, substances are released by the body that tell the brain to initiate the familiar "sickness response," which we have all experienced, for example when we catch the flu. Profound fatigue, headache, sensitivity to light and sound, and painful joints and muscles, drive us to bed. This sickness response forces us to rest and give the body the opportunity to fight the invading germ. This sounds a lot like the symptoms of many Gulf War veterans.

What Dr. Watkins suspects, based on her research on microglia in chronic pain, is that an initial exposure to some toxin "primes" the microglia in the brain to make them hyper alert. Then when a second infection, injury, or toxin is experienced, the brain's immune cells over-react, releasing too much of the chemical signals that cause the "sickness response", and they do not stop releasing the substances after the body heals. In the case of Gulf War veterans, the "initial trigger" could have been a reaction to an immunization, stress, or exposure to low-level toxins. Later a second insult to the body unleashes a run-away illness. Research from several labs on microglia in chronic pain has identified many steps in this neuro-immune signaling process that become disrupted and researchers have found specific drugs to restore the normal function of these pain circuits, thus ending the chronic pain. Most of this work is in laboratory animals but clinical studies are now under way.

In my overview to the committee on the four major kinds of glial cells in "the other brain", several other ways in which glia could be involved in Gulf War illnesses were recognized. This includes the involvement of glial cells, called astrocytes, in processing toxins in the brain. Parkinson's disease, for example can be caused by astrocytes acting on a foreign substance (a recreational drug), and converting it into a toxin that kills the neurons that die in Parkinson's Disease. Astrocytes also release factors that protect neurons from damage caused by inflammation or oxidation, and they release growth factor proteins that stimulate the growth and repair of neurons.

The latest research on the myelin insulation on nerve fibers in the brain, which is essential for sending electrical signals, is revealing a previously unsuspected role of myelin in cognition and psychiatric illness. Myelin insulation is especially vulnerable to blast injuries and to autoimmune diseases in which the body's immune system attacks the myelin sheath. The myelin sheath is made by a type of glial cell, called an oligodendrocyte. Prevously this insulation was of interest in diseases such as multiple sclerosis, but because the insulation speeds the rate of electrical transmission through nerve fibers (axons), myelin is now understood to have an important role in cognitive function, psychological illness, and learning.

One of the reasons the Gulf War Syndrome may have been so difficult to understand is that glia--the other brain--has itself been such a mystery until recently.

Hat tip: THE NICEGUIDELINES BLOG 5/3/10

Professor Hooper's letter to NICE

noreply@blogger.com (Ingrid J. Jones) — Wed, 24 Feb 2010 18:05:00 +0000

From Malcolm Hooper Ph.D.,B.Pharm.,C.Chem.,MRIC
Emeritus Professor of Medicinal Chemistry
19 February 2010

Dear Sir Michael,

I am a ‘blast from your past’. I was at Sunderland School of Pharmacy and you were at Newcastle in Clinical Pharmacology when the M.Pharm course in Pharmacokinetics was developed. Congratulations on your eminent status and knighthood.

Since 1997, when I retired as Professor of Medicinal Chemistry, I have been involved with the emerging and widespread complex chronic multi-system illnesses (Gulf War Syndrome/Illness, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, ME/CFS, multiple chemical sensitivity, MCS, Aerotoxic Syndrome, organophosphate and other pesticide poisonings) that are of growing concern and are medically challenging -- writing and lecturing, locally, nationally and internationally.

This letter is linked to my concerns about ME which involves some 240,000 people in the UK with varying degrees of disability. Some 25% are housebound or bed bound and have formed their own group, www.25megroup.org/ .

The 442 page report “Magical Medicine, how to make a disease disappear”, copy attached with the press release, together with a copy of my letter to the Minister, Lord Drayson, currently the Minister responsible for the MRC, brings together an extensive and fully referenced review of the literature on ME.

It provides the evidence supporting my complaint about the MRC PACE Trial to Lord Drayson.

The entire report, the press release and the letter of complaint have now been circulated worldwide on the internet and have received much acclaim and support from the major ME organisations in various countries and numerous individuals, as well as academic institutions. The report is to be discussed by the International Association of CFS/ME at its next board meeting in early March, as confirmed by the President, Professor Fred Friedberg from the US.

Despite the vast amount of biomedical literature (some 5000 papers) going back to 1934 and the classification of ME as a neurological illness by the WHO (ICD-10 G93.3) since 1969, the official UK attitudes as demonstrated by the MRC, DWP, Department of Health, and to some extent your own organisation NICE:

a. ignore all this evidence
b. show an ideological commitment to a psychosomatic/behavioural model of the illness which is no longer tenable
c. recommend only cognitive restructuring techniques (CBT and GET) that are “not remotely curative” and have been shown to be of no lasting value and in the case of GET to be positively harmful (Peter White’s assertion that this is because the interventions have been incorrectly administered has been shown to lack credibility)
d. proscribe any investigative tests to identify the disorder, leading to missed diagnoses and misdiagnosis
e. support cruel, even vicious, actions that lead to patients being wrongly sectioned and parents, particularly mothers, accused of Munchausens’-Syndrome-by-Proxy, MSBP.
f. the result is that essential benefits and insurance payments to support patients and their families have not been paid or have been granted only after protracted and expensive legal action. All this adds to the burden of the illness for patients and for those who care for them.

The psychiatrists’ argument that what they refer to as “CFS/ME” is substantially different from past epidemics of ME does not withstand scrutiny in the light of current knowledge. It is beyond question that ME is associated with a severely disrupted immune system which renders patients more susceptible to both further viral and chemical challenge and reactivation of latent viruses and persistent viral-specific symptoms.

For the psychiatrists to amalgamate 25 different disorders (Holgate, RSM July 2009) and to focus on “medically unexplained fatigue” whilst ignoring cardinal symptoms of ME is a travesty of medical science.

Of special concern and relevance are the legal and ethical requirements facing doctors today, in particular, the legal requirement for doctors to keep up to date with developments in medicine and medical science (as clearly set out in “Good Medical Practice: Duties of a doctor. The duties of a doctor registered with the General Medical Council: 'Keep your professional knowledge and skills up to date' and 'Never abuse your patients' trust in you or the public's trust in the profession' (http://www.gmc-uk.org/guidance/good_medical_practice/duties_of_a_doctor.asp).

Ignoring vast swathes of evidence is not keeping up to date. For any registered medical practitioner – consultant or GP -- to dismiss or ignore this widely available evidence which invalidates the behavioural model of “CFS/ME”, together with the prescription of inappropriate interventions, is in clear breach of the GMC regulations and consequently raises issues of medical indemnity.

As noted in the report: “since the general body of knowledge known about by other clinicians and researchers working in the field of ME/CFS is now so great, the question repeatedly asked is: at what point will that body of scientific knowledge be so great that it will be considered serious professional misconduct to ignore it and to continue to deceive patients by pretending that it does not exist?”.

The recommendation not to carry out appropriate investigative tests is inconsistent with the Hippocratic Oath in its ancient or modern form.

The offering of treatment that is known even by its proponents to be ineffective is a betrayal of doctors’ responsibility to their patients. Merely to pronounce that the onus is on the individual doctor, when adherence to NICE Guidelines is to become compulsory, is unacceptable.

Inappropriate sectioning of patients and false diagnoses such as MSBP represents a further betrayal.

To rely on only a few studies, showing very modest efficacy, all of which having been shown to have very serious flaws (as is the case with the PACE Trial) and enshrine this inadequate information in official directions, publications and statements from authorised bodies, including NICE, is utterly unacceptable and dishonours the name of medicine as well as being destructive of lives of sick people and those who care for them.

I draw to your attention the commissioned editorial in last week’s BMJ by Alistair Santhouse, who you will be aware was a member of the CG53 GDG. Please read the attached eBMJ response submitted by Horace Reid, a former long-serving NHS clinician.

It was rejected for publication, a fact that is revealing in itself, given that it is impeccably accurate.

I would ask you in your role as Chairman of NICE to engage fully with our report and act accordingly to right the long standing wrongs that people with ME have suffered for the last 20 years.

With best wishes

[With thanks to THE NICEGUIDELINES BLOG]

Official Statement from the Whittemore Peterson Institute Regarding UK Study

noreply@blogger.com (Ingrid J. Jones) — Thu, 07 Jan 2010 16:06:00 +0000

FOR IMMEDIATE RELEASE
Frankie Vigil, 06 January 2010
R&R Partners for Whittemore Peterson Institute
775-336-4555
frankie.vigil@rrpartners.com

Official Statement from the Whittemore Peterson Institute Regarding UK Study

The Whittemore Peterson Institute (WPI) has reviewed the paper entitled “Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome.” This study did not duplicate the rigorous scientific techniques used by WPI, the National Cancer Institute and the Cleveland Clinic, therefore it cannot be considered a replication study nor can the results claim to be anything other than a failure not just to detect XMRV, but also a failure to suggest meaningful results.

The scientific methods used by WPI are very exact and require specific techniques to ensure accuracy. Differences in techniques employed by Erlwein et al. not only explain their failure to replicate the WPI study, but also render the conclusions meaningless. These differences include, but are not limited to the following:

1) blood sample volumes and processing;
2) patient criteria/population differences;
3) number and type of tests done to assure accurate results, including white blood cell culture;
4) use of a molecular plasmid control in water versus a positive blood sample; and
5) different primer sequences and amplification protocol used to find the virus, which were not validated by a clinical control.

The WPI study was published after six months of rigorous review and three independent lab confirmations, proving that contamination had not taken place and that infectious XMRV was present in 67 percent of CFS patients diagnosed according to the Canadian and Fukuda criteria. In contrast, this latest study was published online after only three days of review.

Significant and critical questions remain as to the status of patient samples used in the UK study as those samples may have been confused with fatigued psychiatric patients, since the UK has relegated “CFS” patients to psychiatric care and not traditional medical practices.

“Little is known about the prevalence of XMRV world-wide, much less the incidence of XMRV in ME/CFS or prostate cancer” emphasizes Dr. Judy Mikovits. “WPI and its NCI collaborators are actively engaged with international research teams to investigate these important questions.”

WPI does not recommend the use of anti-retroviral drugs that have yet to be proven to be effective in treating XMRV infection. However, several large pharmaceutical companies have expressed interest in developing anti-retroviral and immune modulating drugs that will effectively treat XMRV associated diseases.

WPI looks forward to the results of other scientific groups around the world, serious about replicating its scientific results, by using the same techniques as WPI and its collaborators. The fact that XMRV was detected in 67 percent of the CFS samples in the U.S. study determined a significant association between XMRV and CFS, demanding a much more serious inquiry by responsible health agencies around the world as to the cause of this debilitating disease.
- - -

Whittemore Peterson Institute
The Whittemore Peterson Institute for Neuro-Immune Disease exists to bring discovery, knowledge, and effective treatments to patients with illnesses that are caused by acquired dysregulation of the immune system and the nervous system, often results in lifelong disease and disability. The WPI is the first institute in the world dedicated to X associated neuro-immune disease (XAND), and other X associated diseases, integrating patient treatment, basic and clinical research and medical education.

'The greater part of nursing consists in preserving cleanliness' -Florence Nightingale

noreply@blogger.com (Ingrid J. Jones) — Wed, 02 Dec 2009 13:28:00 +0000

In her seminal Notes On Nursing, published in 1860, Florence Nightingale wrote that ‘the greater part of nursing consists in preserving cleanliness’.

Hat tip: Melanie Phillips - A diminishing ethic of care

Quote of the Day

The hallmark of a civilised society is the attention paid to the old, infirm and vulnerable. -Melanie Phillips - An uncivilised attitude towards the old

XMRV is a scientific stimulus package for the field of CFS research

noreply@blogger.com (Ingrid J. Jones) — Wed, 02 Dec 2009 13:07:00 +0000

From Facebook by Kim McCleary,
President & CEO The CFIDS Association of America
November 25, 2009
CFIDSLink Extra: Getting "Right" and Giving Thanks

Seven weeks ago, a consortium of researchers at the Whittemore Peterson Institute, Cleveland Clinic and the National Cancer Institute published results of a study linking XMRV, a human retrovirus, and CFS. XMRV had previously been linked to an aggressive form of prostate cancer.

This Oct. 8, 2009 publication in Science continues to attract worldwide media attention and has ignited interest in CFS from many disciplines within the scientific community. As Dr. Daniel Peterson stated at the Oct. 29, 2009 meeting of the federal CFS Advisory Committee, “XMRV is a scientific stimulus package for the field of CFS research.” We couldn’t agree more. Congratulations to the team led by Dr. Judy Mikovits at the Whittemore Peterson Institute and inspired by the Whittemore family, especially Andrea Whittemore-Goad, who has suffered with CFS for 20 years since age 11.

In recent weeks, the U.S. Department of Health and Human Services has formed an interagency task force that is meeting regularly to appropriately replicate the CFS studies, address validation studies, development of appropriate screening and diagnostic tests, and to address the safety of the blood supply. There has not yet been a formal statement from the Department about this interagency effort, but the National Cancer Institute (part of the National Institutes of Health) posted an informational question-and-answer page about XMRV on November 18, 2009. More information from the federal agencies is expected soon, especially on the topic of blood safety.

Numerous follow-up studies are under way at academic centers and government labs in the U.S. and other countries. On November 11, the Cleveland Clinic hosted a meeting of researchers studying XMRV in prostate cancer, CFS, and other diseases. Last week, the Medical Research Council of the U.K. held a meeting on ME/CFS at which XMRV studies were discussed. These investigators are proceeding cautiously to ensure that their results are comparable to the initial study based on the characteristics of patients and controls tested, and the laboratory methods and procedures utilized. Although it’s tempting to pass along rumors about which groups might have found positive and negative results in samples they’ve tested so far, we will await published data from authoritative sources before posting updates.

Response from the CFS community to the initial study, media reports and burgeoning online discourse has run the gamut from salvation to skepticism, from relief to fear, from euphoria to panic. These varied and dynamic reactions have created communications challenges, as organizations and individuals have tried to keep up with the latest news and separate data from opinion and rumor from fact. With the many channels by which people now receive information, new sites have sprung up and existing ones are busier than ever. We’re using a combination of new and traditional media to keep our constituency informed. Content, tone and timing are all important and, at times, we acknowledge that we have gotten only one of the three completely right. And we recognize that these missteps have created some questions and strong feelings about our response to the XMRV study. Be assured that we share the hope and anticipation that these important findings will lead to immediate advances in diagnosis and treatment. And know that we’re listening to feedback, shared both directly and indirectly, with us. We’re constantly working to refine our messages to ensure that we deliver the factual, focused communications you count on.

On this Thanksgiving eve, we express gratitude for the dedicated efforts of all researchers, professionals, and volunteers who seek to advance understanding of CFS, including the team led by the Whittemore Peterson Institute. We are most grateful for the sacrifices of donors at all levels who have sustained the CFIDS Association of America over the past 22 years and who share our relentless determination to make CFS widely understood, diagnosable, curable and preventable.

For more information about the topics mentioned above, please visit http://www.cfids.org/XMRV/default.asp#info.

Warm wishes for a peaceful Thanksgiving holiday.

Kim McCleary
President & CEO
The CFIDS Association of America
November 25, 2009

Meme: Joe Trippi's Eleven-Eleven 1111Campaign - America's and Britain's Veterans have given so much. Now, you can give back.

noreply@blogger.com (Ingrid J. Jones) — Tue, 10 Nov 2009 22:34:00 +0000

Joe Trippi, one of America's greatest bloggers, has launched Eleven Eleven Campaign. The objective of the Eleven Eleven Campaign is simple: to get 11 million Americans to donate $11 to support America’s Veterans. Here is a copy of Joe's latest tweet on Twitter:

Tomorrow is Veterans Day, and now is our moment to encourage our friends, family members and colleagues to join us... http://bit.ly/9Iu9s
33 minutes ago from Facebook
1111Campaign
Eleven Eleven

Hey Joe! Britain's Veterans have given so much too!

Stand with 11 million Brits and Give £11 to Support Britain’s Vets!

Take Action Today
Click here to support Britain's Veterans
November 11, 2009

Top scientists to meet at Cleveland Clinic on trail of XMRV, a suspect in prostate cancer

noreply@blogger.com (Ingrid J. Jones) — Tue, 10 Nov 2009 11:18:00 +0000

Photo: Dr. Robert Silverman is a cancer biologist at the Cleveland Clinic instrumental in the discovery of the XMRV virus. (Lisa DeJong, The Plain Dealer)

From Cleveland.com by Angela Townsend, The Plain Dealer

Tuesday, November 10, 2009
Top scientists to meet at Cleveland Clinic on trail of XMRV, a suspect in prostate cancer

Medical reporter Angela Townsend discusses this story at 7:35 this morning with WCPN FM/90.3’s Eric Wellman on Tuesday Check-up. Listen in or log in online.

The virus XMRV has become a favorite topic in the scientific community -- three years after its initial discovery in prostate cancer tumors by researchers from the Cleveland Clinic and the University of California, San Francisco.

In October, a team of researchers from the Clinic, the University of Nevada at Reno and the National Cancer Institute reported finding the virus in the majority of patients they studied who had chronic fatigue syndrome. CFS is a debilitating disorder marked by profound fatigue, muscle pain, impaired memory and other symptoms. Its causes are unknown.

That news came on the heels of another study, published in September, that revealed the virus could be an important marker for aggressive prostate cancer tumors.

Capitalizing on the excitement and heightened spirit of collaboration, 75 of the top scientists nationwide studying XMRV are flying in to convene Wednesday at the Clinic.

"This is the first meeting of the major players in the area of XMRV," said John Coffin of the department of microbiology at Tufts University in Boston. "I think there's going to be a lot of excitement and a lot of new information presented."

XMRV is one of three known human retroviruses. The other two are HIV and HTLV (a type of virus that infects white blood cells and can cause leukemia and lymphoma). All three are transmitted through bodily fluids.

One of the most striking things about XMRV is that there are indications that up to 4 percent of people in the United States carry the virus, said Coffin, who wrote an editorial accompanying a journal article on the link to chronic fatigue syndrome.

"There might be other consequences of this infection," he said.

The invitation-only gathering will be the first large meeting of scientists on XMRV since the National Institutes of Health's closed-door session last summer on the topic.

The National Cancer Institute helped pull together key people involved in various research projects, said Robert Silverman, a cancer biologist at the Clinic's Lerner Research Institute. "It's been about two months in the making."

It will be a chance for researchers not only to swap information but to form new collaborations.

"We're learning things at such a rapid pace that we need a venue to exchange ideas and information," said Dr. Ila Singh, a professor in the University of Utah's department of pathology and senior author of the research involving prostate cancer patients.

"I'm hoping for a deeper understanding. We know so little at the moment. I'm hoping to learn more about the virus," she said. "That's what's sorely lacking. There's a lot of speculative information . . . I want to know what's real."

In advance of Wednesday's meeting, Silverman, one of the researchers credited with the initial discovery of XMRV, spoke with The Plain Dealer:

How did XMRV get its name?

It's a descriptive name. Xenotropic, which means the virus came from mice but mice are immune to its effects. It does affect other animals. Murine leukemia, which is the parent virus. Related Virus.

How does XMRV affect animals?

XMRV is closely related to a virus that causes leukemia, lymphoma and neurological diseases in animals. [Research] suggests that the human version could cause similar disease.

How did humans acquire XMRV?

We probably acquired it from mice because that's where the prototype exists. At what point it crossed over to humans we don't know. It's probably something that's been out there for a long time. Maybe many years.

How is XMRV spread?

That research is in the planning stage. What we're doing is trying to develop diagnostic assays to assess who has it and who doesn't. We're trying to determine how the virus is transmitted.

With the new possible link to chronic fatigue syndrome, does this make getting funding for XMRV research easier?

The funding part remains to be seen. There's been a tremendous interest in chronic fatigue syndrome. I've been getting almost nonstop calls from doctors and patients. They're obviously looking for hope in this study, although the virus is not proven to cause CFS. That's still unknown. But until it's ruled out, it's going to obviously be a subject of great interest.

Have the research gains since your findings three years ago been significant enough that investigators are hopeful about what may be around the corner?

It was kind of a sleeper. We published in 2006. There were really only a handful of papers published in the first couple years. It takes time for scientists to mobilize and perform research. Now there's a flurry of publications working on it. The field is exploding. It depends on whether we can nail down if this is a disease-causing virus. The potential of this is enormous. If it is proven to cause prostate cancer or chronic fatigue syndrome, then there would be the potential for new methods of diagnosis, new methods of treatment -- antivirals, even for prevention. That's why we're so excited about the prospect.

What about the recent study by German researchers in the journal Retrovirology that found no link between XMRV and prostate cancer?

It is not atypical of science for different groups to get different results. There could be methodological differences. I believe our methods were more sensitive. They may have missed it. Or it could be a different strain. Another interpretation is that the virus is more prevalent in the United States than in Germany.

Why should the average person care about XMRV?

We don't know at this point if the virus causes either prostate cancer or chronic fatigue syndrome. Our results suggest that XMRV is a candidate for causing human disease. However, it's still in a relatively early stage of the research. There are potentially major public health implications of this virus, so there's an urgency to figure it out and move forward.

What is the Clinic working on now in relation to XMRV?

We're working to help develop a diagnostic test that could be applied to a large number of people. It could be developed pretty quickly, maybe in a year or two.

We're really studying how the virus could cause disease at a very fundamental level. But a vaccine could be 10 years [away] or maybe longer.

This is exciting research. We're working as hard as we can to help benefit patients.

Contact Angela Townsend: atownsen@plaind.com or 216-999-3894.

Salute Royal British Legion & Combat Stress - Remembering PTSD and GWS on Remembrance Sunday

noreply@blogger.com (Ingrid J. Jones) — Sun, 08 Nov 2009 11:43:00 +0000

Today, on Remembrance Sunday, while watching BBC1 TV coverage of the memorial ceremony from the Cenotaph in Whitehall, London, I heard the presenter, David Dimbleby, remark on a 10% increase in requests for help from Combat Stress, an ex-services mental welfare society set up to help ex-service personnel suffering from psychological injuries and mental problems.

+ + + Remembrance Sunday &
The 11th hour of the 11th day of the 11th month + + +

Photo: Remembrance Day Poppy

Two minutes of silence at the eleventh hour of the eleventh day of the eleventh month because that was the time (in Britain) when the armistice became effective. The two minutes recall World War I and World War II. Before 1945 the silence was for one minute, and today some ceremonies still only have one minute of silence despite this.

In the United Kingdom, although two minutes' silence is observed on November 11 itself, the main observance is on the second Sunday of November, Remembrance Sunday.

Source: Remembrance Day - Wikipedia

POST TRAUMATIC STRESS DISORDER (PTSD)

See my blog Sudan Watch, 10 October 2008: Deployed peacekeeping veterans with Post Traumatic Stress Disorder (PTSD) have significant impairments in health-related quality of life

PTSD: Bonfire Night Cartoon

noreply@blogger.com (Ingrid J. Jones) — Fri, 06 Nov 2009 09:37:00 +0000

'I've got PTSD.'
- - -

POST TRAUMATIC STRESS DISORDER (PTSD)

Incase a VIP from the MOD ever comes across this blog post: please see my blog Sudan Watch, 10 October 2008: Deployed peacekeeping veterans with Post Traumatic Stress Disorder (PTSD) have significant impairments in health-related quality of life

Ampligen, the proposed chronic fatigue syndrome drug currently awaiting FDA approval

noreply@blogger.com (Ingrid J. Jones) — Thu, 29 Oct 2009 11:02:00 +0000

From Fibromyalgia & CFS Blog, 29 October 2009
By Adrienne Dellwo, About.com Guide to Fibromyalgia & CFS

Chronic Fatigue Syndrome: Dr. Lerner on Ampligen, XMRV

Dr. A Martin Lerner: Thoughts on XMRV, Ampligen

In my recent conversation with Dr. A. Martin Lerner, a former chronic fatigue syndrome sufferer who says he used his specialty in infectious diseases to find treatments for himself and others, I asked him about both the XMRV discovery (which was just days old at the time) and also aboutAmpligen, the proposed chronic fatigue syndrome drug currently awaiting FDA approval.

XMRV

XMRV is a retrovirus that researchers recently linked to chronic fatigue syndrome (CFS or ME/CFS). Dr. Lerner says that in his patients, he's discovered that 3 viruses are found in nearly everyone with ME/CFS -- Epstein-Barr virus (EPV), human herpesvirus 6 (HHV-6) andcytomegalovirus (CMV) -- and that some patients also have Lyme disease on top of one or more of those viruses.

At the time of our conversation, Dr. Lerner hadn't yet been able to look over the XMRV data but said he was definitely interested in seeing it.

On the surface, it might seem like other research -- especially the XMRV finding -- could disprove Dr. Lerner's theories about EBV, HHV-6 and CMV. However, (and these are my words, not his) that's not necessarily true. If the XMRV findings are replicated and nearly everyone with ME/CFS is infected with it, that wouldn't meant that other infectious agents didn't play a role. Could XMRV make people more susceptible to complications/long-term infection by EBV, HHV-6 or CMV? Could EBV, HHV-6 and CMV make us more vulnerable to XMRV infection? These are all areas that researchers could explore in the future.

Ampligen

Dr. Lerner treats his ME/CFS patients with one of two antiviral medications:

I asked him about Ampligen, which many hope will become the first drug ever approved for ME/CFS. "The science behind Ampligen is sound," Dr. Lerner said. He doesn't use it because it has to be given intravenously, which means patients have to come to the office more often, whereas people can take the other two at home.

Dr. Lerner and I also talked a lot about exercise in people with chronic fatigue syndrome, and he has a very interesting take on it. That's coming up soon.

More on Dr. Lerner

Comments

October 29, 2009 at 6:19 am (1) Mindy Leavell says:: Adrienne, Check out this website. http://www.codiagnostics.com/XMRV/index2.php
They say they have a diagnostic test available for XMRV…..?

XMRV: Reno scientists prepare to address federal health officials

noreply@blogger.com (Ingrid J. Jones) — Thu, 29 Oct 2009 08:47:00 +0000

Annette Whittemore, founder and president of Whittemore Peterson Institute (WPI), will also speak at the meeting.

WPI will open a permanent research facility next June at the University of Nevada, Reno, USA.

From News 4 by Victoria Campbell, 29 October 2009:
Reno scientists prepare to address federal health officials

Just weeks after a medical breakthrough that pinpointed a virus that may be linked to Chronic Fatigue Syndrome, the doctor who helped lead the medical team is preparing to present his findings to an advisory committee from the U.S. Department of Health and Human Services.

Dr. Daniel Peterson, medical director of the Whittemore Peterson Institute at the University of Nevada, Reno, will discuss the findings before the Chronic Fatigue Syndrome Advisory Committee on Thursday, October 29, in Washington, D.C.

Dr. Peterson has treated patients with Myalgic Encephalomyelitis-commonly known as Chronic Fatigue Syndrome-for more than 25 years. Earlier this month, scientists at WPI identified an infectious retrovirus they called XMRV that could be linked to the devastating condition that affects millions of people worldwide.

Dr. Peterson said the discovery by scientists at WPI holds great promise for patients all over the world.

"I am hopeful about the possibility of providing patients who are positive for XMRV a definitive diagnosis, and hopefully very soon, a range of effective treatment options," he said.

Annette Whittemore, founder and president of WPI, will also speak at the meeting. WPI will open a permanent research facility next June at the University of Nevada, Reno.

MEA writes to the Chief Medical Officer - Implications of research findings concerning XMRV and ME/CFS

noreply@blogger.com (Ingrid J. Jones) — Tue, 27 Oct 2009 20:00:00 +0000

From the M.E. Association's website by Dr Charles Shepherd, 27 October 2009:

XMRV and ME/CFS: The MEA writes to the Chief Medical Officer

The ME Association has today written to Sir Liam Donaldson, Chief Medical Officer at the Department of Health, about various issues relating to XMRV research and ME/CFS.

Dear Sir Liam

Implications of research findings concerning XMRV and ME/CFS

I assume you are aware of the new research findings from America, published in Science on 8 October 2009, which relate to the retrovirus known as XMRV (xenotropic murine leukaemia virus) and ME/CFS.

The ME Association has produced some information which summarises the research findings and the practical implications they may have in relation to disease management. Our position statement acknowledges that many uncertainties remain and that further research studies are needed before anyone can conclude that this virus plays a significant role in either the cause, assessment or management of ME/CFS. We are in contact with several research groups (UK and overseas) who have experience in retroviral research and it is encouraging to note that there is a strong desire in the research community to take this forward as a matter of urgency. I can supply further information if necessary. The ME Association summary, which also contains a link to the XMRV research paper, can be found on our website at: www.meassociation.org.uk/content/view/1051/213

I would also like to draw your attention to two statements that have been issued by the National Cancer Institute in America in relation to XMRV. The first statement, which refers to the research findings, can be found at: http://www.cancer.gov/newscenter/pressreleases/CFSxmrv The second statement, which refers to transmission and blood donation, can be found at:http://www.cfids.org/temp/xmrv-guidelines-nci.asp. The NCI interim guidelines relating to blood donation in the second statement (>> point 2) are very similar to those contained in the MEA summary, and the issue of XMRV transmission is something that obviously needs to be brought to the attention of the National Blood Service and Health Protection Agency if not already done so. A clear statement from the National Blood Service in relation to blood donation from people with ME/CFS would obviously be very helpful to people at this time.

If the Department of Health, or the National Blood Service, would like to add anything to the MEA information, which is being updated at regular intervals, we would be happy to include it.

Yours sincerely

Dr Charles Shepherd

Honorary Medical Adviser, The ME Association

7 Apollo Office Court

Radclive Road

Gawcott

Bucks MK18 4DF

Formerly a member of the CMO Working Group on ME/CFS

Copies:

Dr Des Turner MP - Chair of the All Party Parliamentary Group on ME

Countess of Mar - Chair of Forward ME Group

Dr Jonathan Stoye - National Institute for Medical Research

Professor Stephen Holgate - Chair of MRC Expert Group on ME/CFS Research

Professor Tony Pinching - Peninsular Medical School

News round-up: Whittemore Peterson Institute for neuro-immune disease (Update 1)

noreply@blogger.com (Ingrid J. Jones) — Fri, 23 Oct 2009 10:45:00 +0000

In The News

October 9, 2009: Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome (Science)

View Abstract | View Reprint | View Full Citation

Does a Virus Cause Chronic Fatigue? ABC News, October 19, 2009
Consortium of Researchers Discover Retroviral Link to Chronic Fatigue Syndrome(NIH/National Cancer Institute Press Release, October 8, 2009)
Whittemore Peterson Institute Scientists Discover Significant link between XMRV and ME/CFS (WPI Press Release; October 8, 2009) [PDF]
Virus Linked To Chronic Fatigue Syndrome (NPR, October 8, 2009)
Virus Found in Many With Chronic Fatigue Syndrome (NYTimes.com, October 8, 2009)
ME virus discovery raises hopes (BBC NEWS | Health, October 9, 2009)
Retrovirus Might Be Culprit In Chronic Fatigue Syndrome (Science News, October 8, 2009)
Chronic fatigue caused by retrovirus, say scientists (Mail Online, October 10, 2009)
'Most cases of chronic fatigue syndrome linked to virus' (Telegraph, October 9, 2009)
Retrovirus May Be at Root of Chronic Fatigue Syndrome (US News and World Report, October 8, 2009)
Retrovirus Linked to Chronic Fatigue Syndrome (WebMD, October 8, 2009)
Study isolates virus in chronic fatigue sufferers (Reuters, October 8, 2009)
Chronic fatigue linked with virus (The Australian, October 10, 2009)

September 24, 2009: WPI Awarded Prestigious NIH R01 Grant
New Strategies to Decipher the Pathophysiology of Chronic Fatigue Syndrome

February 4, 2009: New UNR Center Raises Hopes for CFS Patients
Reno Gazette-Journal [PDF]

Summer, 2008: Whittemore Family Invests in Neuro-immune Institute
Nevada Silver & Blue [PDF]

Summer, 2008: Center for Molecular Medicine Targets Chronic Fatigue Syndrome
Nevada Silver & Blue [PDF]

Healthcare Heroes
Annette and Harvey Whittemore, Northern Nevada, Community Partner
Nevada Business Journal report [PDF; see page 20]

INIP award
September 8, 2007: NCI CCR (Ruscetti)/NIA (Taub) proposal submitted to the Integrative Neural Immune Program's Intramural Research Award competition, entitled "Role of Chronic Inflammatory Stimulation by Active Herpesvirus Infection in Development of Immune Dysfunction and Mantle Cell Lymphoma in Chronic Fatigue Syndrome Patients", unanimously considered by the ad hoc reviewers and the INIP IRA subcommittee as a project that will yield important new interdisciplinary research findings. The award provides a postdoctoral fellow for 3 years to work on the Project with Dr. Ruscetti and Dr. Taub and WPI.

- - -

News round-up from ME agenda

Whittemore Peterson Institute XMRV retrovirus study link with CFS: Media Round up 10

Posted by meagenda on October 17, 2009

Whittemore Peterson Institute XMRV retrovirus study link with CFS (Science journal): Media Round up 10

WordPress Shortlink: http://wp.me/p5foE-2bk

This is the tenth Round up of media coverage of the Whittemore Peterson Institute XMRV study published, last week (08.10.09), in Science journal. Round ups also include commentary from patient organisations, patient community websites and bloggers and links for related material.

Press Release:

The European ME Alliance www.europeanmealliance.org

Eight-Country European ME Alliance Issues Kudos to WP Institute, Pledges Cooperation
October 16, 2009

The European ME Alliance www.europeanmealliance.org is a group of European organizations formed less than a year ago to encourage more ME/CFS biomedical research funding – Belgium, Denmark, Ireland, Germany, Norway, Sweden & UK.
__________________

ME Alliance Press Release Oct 16:

The European ME Alliance (EMEA) wish to congratulate the Whittemore- Peterson Institute for the painstaking, professional and groundbreaking work which its staff have performed, along with the National Cancer Institute and the Cleveland Clinic, which has resulted in the publication of the findings of a novel virus XMRV in causing or influencing ME.

The members of EMEA recognize that the staff at WPI are performing research of the highest quality.

The publication of this research in Science magazine is itself an amazing achievement.

This work has been achieved in an amazingly short period of time and the tenacity, dedication and sheer excellence of the WPI has brought hope to millions of people, patients, carers and friends, in Europe and further afield.

EMEA announces its continued full support for WPI and hopes to be able to become a stronger partner in the future.

Signed by all members of the European ME Alliance:

Belgium – ME/CFS Association (Nieuwrode, Belgium)
Denmark – ME-NetDK
Ireland – Irish ME Trust
Germany – Fatigatio e.V.
Norway – Norges ME-forening
Spain – Liga SFC
Sweden – Riksföreningen för ME-patienter
UK – Invest in ME

The European ME Alliance
www.europeanmealliance.org

——————–

Tate Mitchell reports via Co-Cure mailing list 16 October 2009

“The CFIDS Assoc. just posted some updates on their Facebook page, including a link to an interview with Laura Hillebrand, author of Seabiscuit, by The New Yorker, the Oct. 29-30 CFSAC meeting agenda is published, which is to include a presentation by Dr. Daniel Peterson entitled ‘XMRV Association with CFS’, and CFIDS Assoc. Scientific Director Suzanne Vernon writes about the new XMRV findings”

http://www.facebook.com/CFIDSAssn

Oct. 29-30 CFSAC agenda

http://www.hhs.gov/advcomcfs/meetings/agendas/cfsac091029_agenda.html

Interview with Laura Hillebrand

http://www.newyorker.com/online/blogs/backissues/2009/10/back-issues-laura-hillenbrand.html

—————–

Commentary

http://www.facebook.com/note.php?note_id=185660730538&ref=mf

http://www.cfids.org/cfidslink/2009/110402.asp

Xplained

By Suzanne D. Vernon, PhD
Scientific Director, The CFIDS Association of America

The announcement on October 8, 2009, that an infectious retrovirus called XMRV (xenotropic murine-related retrovirus) was linked to CFS, could be the game-changing scientific event we have been waiting for. Whether XMRV provides the long-awaited causal link will depend on the findings described in the Science paper being replicated by another laboratory in another group of CFS patients. To help clarify what we know, let’s review the findings.

Dr. Judy Mikovits and her team at the Whittemore Peterson Institute for Neuro-immune Disorders (WPI) made a very insightful connection three years ago. XMRV was first described in prostate cancer in 2007 by investigators at the Cleveland Clinic, who also reported that XMRV-positive prostate cancer patients have alterations in RNase L, an antiviral immune system pathway. The WPI investigators knew that RNase L activity is also altered in blood cells from CFS patients and they made the decision to look for XMRV in CFS patients with this immune defect.

When scientists want to find a virus, we look for it in the sickest individuals because often this is where there is likely to be the highest levels of a virus, if present. Dr. Dan Peterson has been caring for and researching CFS patients since the 1984 Incline Village outbreak, so he identified CFS patients with prolonged disabling fatigue, cognitive impairment, and documented laboratory immunological abnormalities (including altered RNase L activity) to hunt for XMRV.

The WPI laboratory team detected XMRV sequences in 68 of 101 (67%) CFS patients tested and in 8 of 218 (3.7%) healthy control subjects. The Cleveland Clinic confirmed the presence of XMRV in a subset of these same CFS cases, 7 of the 11 (64%) samples from WPI. The Cleveland Clinic researchers found that the CFS XMRV was similar to prostate cancer XMRV, and not a mouse virus (murine leukemia virus) that could have been a contaminant explaining the discovery.

The investigators designed several new assays to understand XMRV. They looked to see if XMRV was expressed in peripheral blood mononuclear cells (PBMCs) of CFS patients. PBMCs from 19 of 30 CFS patients expressed XMRV proteins compared to 0 of 16 PBMC samples from healthy controls. They also wanted to know which cells harbored XMRV; they found it in T and B cells in the blood of one CFS patient. The investigators looked to see if the XMRV from CFS patients was infectious. Both blood cells and plasma (the cell-free fraction of blood) from XMRV-positive CFS patients were able to transmit this virus to a susceptible cell line, indicating infectiousness in laboratory culture. Finally, they wanted to know if XMRV stimulated the immune system to produce antibodies. Plasma from 9 of 18 CFS patients had antibodies that reacted with a virus protein similar to that found in XMRV, compared to no reaction from plasma of 7 healthy controls.

This Science paper tells us that XMRV plays a possible role in CFS pathogenesis in these CFS patients. How much we can generalize these findings to other CFS patient populations? That answer will depend on the results of replication studies.

The design of replication studies should include CFS patients who are similar to those selected by Dr. Peterson and reported in the Science study. Unfortunately, the details about the CFS patients were not sufficient to enable independent investigators to select similar CFS patients. For example, we need to know the age, sex, duration of illness, medical history, and medication use, to name a few characteristics, of the studied patients to select CFS patients who as similar as possible to the original group. We also need to know something about the healthy control subjects, since there is nothing in the paper or supplementary materials that describes how they were selected. Independent replication studies should also include patients with mild and moderate CFS, at least one chronic disease control group (e.g., multiple sclerosis, lupus) and sex and age-matched healthy controls. We are actively working with several independent research groups to expedite these studies.

While these exciting studies of XMRV continue, the CFIDS Association continues its support of our funded investigators. It’s important to remember that HIV was discovered to be the cause of AIDS 26 years ago, but worldwide research on AIDS treatment, cure and prevention continues today. Our funded investigators’ research on why EBV triggers CFS, whether ion-channel receptors are markers of fatigue, why CFS patients have higher rates of leaky gut, why CFS patients have slow blood flow to the brain, why CFS patients have metabolic disturbances in the brain, and how we can bring this information, as well as XMRV, together using powerful computational tools are all important as we work together to solve CFS.

References:
Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Lombardi VC, Ruscetti FW, Gupta JD, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. Science 8 October 2009. 1179052.

Supporting online material for Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Lombardi VC, Ruscetti FW, Gupta JD, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. Science 8 October 2009.

A new virus for old diseases? Coffin JM and Stoye JP. Science 8 October 8 2009.

Information about the Association’s research program:
http://www.cfids.org/about/acceleratecfsresearch.asp

—————–

Commentary

Professor Andrew Lloyd AM
Director, Centre for Infection and Inflammation Research University of New South Wales

http://www.me-cfs.org.au/node/448

New Retrovirus – Comments by Professor Andrew Lloyd

—————–

Commentary

RESCIND would like to emphasize what we feel are probably the two most powerful quotes on record in M.E. (C.F.S.) history…

Dr. Nancy Klimas as quoted from the Q & A New York Times article “Is a Virus the Cause of Fatigue Syndrome?” – posted online Oct 15, 2009

http://consults.blogs.nytimes.com/2009/10/15/readers-ask-a-virus-linked-to-chronic-fatigue-syndrome/

“But I hope you are not saying that C.F.S. patients are not as ill as H.I.V. patients. My H.I.V. patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested. Many of my C.F.S. patients, on the other hand, are terribly ill and unable to work or participate in the care of their families. I split my clinical time between the two illnesses, and I can tell you if I had to choose between the two illnesses (in 2009) I would rather have H.I.V.”

Dr. Marc Loveless as quoted by Tom Hennessy from A Brief History of the Name Change Movement

http://www.rescindinc.org/history.htm

Dr. Shelekov looked puzzled and maybe a little skeptical. But Dr. Marc Loveless, sitting next time to him said, “Dr. Shelekov, this man (meaning me) is telling you the truth. I have treated more than 2500 AIDS and CFS patients over the past 12 years. and my CFS patients are MORE sick and MORE disabled, every single day, than my AIDS patients are, except in the last two weeks of life!”

I immediately said to Dr. Loveless that “YOU have to use that line in every speech you give on this illness for the rest of your life!” (in 1994, Dr. Loveless gave this same testimony under oath to the US Congress).

——————–

Radio broadcasts

Science Friday on NPR

“Science Friday is a weekly science talk show, broadcast live over public radio stations nationwide from 2-4pm Eastern time as part of NPR’s ‘Talk of the Nation’ programming.”

http://www.sciencefriday.com/about/listen/

Podcast: Virus Tied to Chronic Fatigue Syndrome

Clicking on this link will start download of mp3 Podcast from Science Friday site:

http://podcastdownload.npr.org/anon.npr-podcasts/podcast/510221/113890711/npr_113890711.mp3

——————–

Patient community websites and blogs

Cort Johnson’s Phoenix Rising website

http://aboutmecfs.org/Rsrcs/XMRVResources.aspx

The news on XMRV is breaking fast and items are being added regularly to the XMRV Resource Center on Phoenix Rising. The Resource Center has links to scientific articles, analyses by chronic fatigue syndrome specialists (check out the video by Dr. Klimas on CFSKnowledge Center), media reports, Q&A’s, blogs and more.

Hillary Johnson (journalist and author of Osler’s Web)

Website: http://oslersweb.com/

Blog: http://oslersweb.com/blog.htm

——————–

Links to scientific coverage

Whittemore Peterson Institute Q and A
Whittemore Peterson Institute Press Release
Science News: Retrovirus might be culprit in chronic fatigue syndrome
New Scientist: Chronic fatigue syndrome linked to ‘cancer virus’
Scientific American: Retrovirus Linked to Chronic Fatigue Syndrome, Could Aid in Diagnosis
Nature: Virus linked to chronic fatigue syndrome
NIH News: Consortium of Researchers Discover Retroviral Link to Chronic Fatigue Syndrome

——————–

Previous ME agenda Media Round ups

Round up 10: Whittemore Peterson Institute XMRV retrovirus study link with CFS (Science journal):
http://wp.me/p5foE-2bk

Round up 9: Notice from Dr David Bell, Lyndonville News; Article by Paul R. Cheney MD, PhD:
http://wp.me/p5foE-2aQ

Round up 8: XMRV retrovirus study: Position statement from ME Association 14.10.09:http://wp.me/p5foE-2at

Round up 7: XMRV Retrovirus: Whittemore Peterson Institute: CFS: Media Round up 7:http://wp.me/p5foE-2aa

Round up 6: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study: Videos and audios: http://wp.me/p5foE-29L

Round up 5: Supporting Online Material for XMRV Chronic Fatigue Syndrome study: http://wp.me/p5foE-299

Round up 4: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study:
http://wp.me/p5foE-28F

Round up 3: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome retrovirus XMRV in the media: http://wp.me/p5foE-280

Round up 2: Science 9 October 2009: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 08.10.09: http://wp.me/p5foE-27v

Round up 1: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 09.10.09:http://wp.me/p5foE-272

APPG on ME launches legacy paper consultation 22 Oct 2009

noreply@blogger.com (Ingrid J. Jones) — Thu, 22 Oct 2009 14:54:00 +0000

APPG on ME launches legacy paper consultation

A consultation on the Legacy Paper for the All Party Parliamentary Group (APPG) on M.E. was launched yesterday (October 22).

The current Chair of the APPG, Dr Des Turner, intends to stand down at the next General Election, due sometime before 3 June 2010.

Comments on the draft APPG legacy paper should be sent to the Secretariat no later than 19 November 2009.

The Countess of Mar, who is Secretary of the Group, thanked people with M.E. and Action for M.E. for the work done so far in producing the draft.

The main speaker at the meeting was the Rt Hon Yvette Cooper MP, Secretary of State for Work and Pensions, who described her own personal experience of M.E. and answered a number of questions. In particular, she reassured people with M.E. that it was not the Government’s intention to change working-age Disability Living Allowance under current care reform proposals.

Other topics on the agenda included an update on the APPG Inquiry into NHS services, which is expected to produce a report before the next meeting of the APPG, which will take place on Wednesday 2 December 2009. A Minister from the Department of Health would be invited to attend.

In addition to the Chair, Dr Turner and the Secretary, the Countess of Mar, the meeting was attended by Vice Chairs Andrew Stunell MP and Tony Wright MP (Vice Chairs), plus Bill Wiggin MP and Russell Brown MP.

Minutes and a transcript of the meeting will be produced in due course.

SOURCE: Website of The M.E. Association (UK)

PVFS/ME/CFS Watch

Research paper: CFS, the immune system and viral infection, 2 July 2011

What's it like to have severe ME/CFS? It's a living death and hell in solitary confinement

New study: Gene expression alterations at baseline and following moderate exercise in patients with CFS & FMS

The US National Institutes of Health is sponsoring new studies to ascertain whether the association between XMRV and CFS can be confirmed

Viral Encephalomyelitis - Academic review

Virology: Nature News Feature - XMRV could be an opportunistic infection affecting those whose immune systems are already dampened by CFS/ME

Chronic Neuroimmune Diseases - CFS: A polio by another name

Dorset woman with severe ME 'left to rot by the NHS'

Related stories

CFS: XMRV could be a 'rumour virus' - Where have the epidemiologists been all this time? I am an emergency doctor and this is an emergency!

Abundant Evidence ME/CFS is Neurological - Harvard's Dr. Komaroff

April 12, 2010: Whittemore Peterson Publicly Challenges UK Researchers to Collaborate on XMRV & ME/CFS Research

New Suspect In Gulf War Syndrome

Professor Hooper's letter to NICE

Official Statement from the Whittemore Peterson Institute Regarding UK Study

'The greater part of nursing consists in preserving cleanliness' -Florence Nightingale

XMRV is a scientific stimulus package for the field of CFS research

Meme: Joe Trippi's Eleven-Eleven 1111Campaign - America's and Britain's Veterans have given so much. Now, you can give back.

Top scientists to meet at Cleveland Clinic on trail of XMRV, a suspect in prostate cancer

Salute Royal British Legion & Combat Stress - Remembering PTSD and GWS on Remembrance Sunday

PTSD: Bonfire Night Cartoon

Ampligen, the proposed chronic fatigue syndrome drug currently awaiting FDA approval

Chronic Fatigue Syndrome: Dr. Lerner on Ampligen, XMRV

XMRV: Reno scientists prepare to address federal health officials

MEA writes to the Chief Medical Officer - Implications of research findings concerning XMRV and ME/CFS

News round-up: Whittemore Peterson Institute for neuro-immune disease (Update 1)

Whittemore Peterson Institute XMRV retrovirus study link with CFS: Media Round up 10

Press Release:

Commentary

Radio broadcasts

Patient community websites and blogs

Related links

Links to scientific coverage

Previous ME agenda Media Round ups

APPG on ME launches legacy paper consultation 22 Oct 2009

PVFS/ME/CFS Watch

Research paper: CFS, the immune system and viral infection, 2 July 2011

What's it like to have severe ME/CFS? It's a living death and hell in solitary confinement

New study: Gene expression alterations at baseline and following moderate exercise in patients with CFS & FMS

The US National Institutes of Health is sponsoring new studies to ascertain whether the association between XMRV and CFS can be confirmed

Viral Encephalomyelitis - Academic review

Virology: Nature News Feature - XMRV could be an opportunistic infection affecting those whose immune systems are already dampened by CFS/ME

Chronic Neuroimmune Diseases - CFS: A polio by another name

Dorset woman with severe ME 'left to rot by the NHS'

Related stories

Related Internet links

Around the BBC

CFS: XMRV could be a 'rumour virus' - Where have the epidemiologists been all this time? I am an emergency doctor and this is an emergency!

Abundant Evidence ME/CFS is Neurological - Harvard's Dr. Komaroff

April 12, 2010: Whittemore Peterson Publicly Challenges UK Researchers to Collaborate on XMRV & ME/CFS Research

New Suspect In Gulf War Syndrome

Professor Hooper's letter to NICE

Official Statement from the Whittemore Peterson Institute Regarding UK Study

'The greater part of nursing consists in preserving cleanliness' -Florence Nightingale

XMRV is a scientific stimulus package for the field of CFS research

Meme: Joe Trippi's Eleven-Eleven 1111Campaign - America's and Britain's Veterans have given so much. Now, you can give back.

Top scientists to meet at Cleveland Clinic on trail of XMRV, a suspect in prostate cancer

Salute Royal British Legion & Combat Stress - Remembering PTSD and GWS on Remembrance Sunday

PTSD: Bonfire Night Cartoon

Ampligen, the proposed chronic fatigue syndrome drug currently awaiting FDA approval

Chronic Fatigue Syndrome: Dr. Lerner on Ampligen, XMRV

XMRV: Reno scientists prepare to address federal health officials

MEA writes to the Chief Medical Officer - Implications of research findings concerning XMRV and ME/CFS

News round-up: Whittemore Peterson Institute for neuro-immune disease (Update 1)

Whittemore Peterson Institute XMRV retrovirus study link with CFS: Media Round up 10

Press Release:

Commentary

Radio broadcasts

Patient community websites and blogs

Related links

Links to scientific coverage

Previous ME agenda Media Round ups

APPG on ME launches legacy paper consultation 22 Oct 2009