Searching for Answers

We're spending billions to develop an HIV vaccine. Why not also focus on building a better condom?

2012-02-23T19:58:00.000-08:00

Condoms Suck

www.laweekly.com

Imagine you're trying to hook up with a date, and he whips out a circa-1999 cellphone. Date over.

Now imagine the evening is going well — really well — and your companion whips out a circa-1799 condom. Date normal.

Condoms, the medical contemporaries of bloodletting and leeches, have not been significantly improved since the 1800s, when rubber first replaced the then-standard animal intestines, which were an upgrade from leather.

We can do better, people.

Condoms suck. Having to put a tight, sensation-stealing plastic trash bag over your johnson during sex sucks. And yes, sexually transmitted infections suck, too, but not badly enough, apparently, even with the threat of serious illness and death, to get everyone to use condoms every time. Admit it: You don't use a condom every time.

Even doctors don't use condoms every time. A conversation with a USC professor of medicine provoked a hush-hush confession that at least a dozen fellow physicians suffered from sexually transmitted infections — HIV, genital herpes, the gamut. Such infections may be more common in less educated populations, but they're far from nonexistent in academia. If doctors, who have seen firsthand the ravages of such infections, can't reliably use condoms, what hope is there for the rest of humanity?

It's easy to blame the risk takers among us, to dismiss them as impulsive, impoverished and uneducated, but condoms suck whether or not you've got an advanced degree. It's time to look for another place to put the blame.

And it's not with the manufacturers. Condoms are a high-volume, low-cost product, so the businesses that produce them, understandably, put money into distribution, not innovation. They might tinker with shapes, adding "pleasure ribs" or even minivibrators, but game-changing innovation takes a wad of cash that condom makers just don't have.

Take Carter-Wallace, the New York–based company that owned the premier condom brand Trojan for decades. When Carter-Wallace sold its consumer division in 2001, it was worth just $739 million — and that included not just Trojan but also Arrid deodorant and other brands.

Contrast that with the number of Benjamins we've thrown at developing an HIV prevention vaccine: $682 million in 2004 alone, according to a 2005 study funded in part by the Joint United Nations Programme on HIV/AIDS. A huge chunk of that funding — 88 percent — came from the public sector, with the United States kicking in $2.5 billion from 2000 to 2005. Wealthy donors also have been motivated to help: Bill Gates alone has contributed $4.5 billion to vaccines. None of that money went to condom tech.

Yet, although we've been chasing an HIV-prevention vaccine since 1984, we've still got nothing to show for it. Imagine how far those same hundreds of millions could go toward the development of a better-feeling condom — a condom people would actually wear.

After all, there is one area in which condoms don't suck: They prevent sexually transmitted infections. To date, we haven't even found a vaccine to prevent one of the many strains of HIV. Even if an omnipotent AIDS vaccine were developed, it would still leave untouched syphilis, gonorrhea, chlamydia and every other sexually transmitted infection. Compare that to the simplicity of the one-size-fits-all-diseases barrier method: the simple condom.

Chasing a vaccine has so far been a losing game. But a great-feeling condom could be an epic win.

Here's the dirty little secret of condoms: They actually were meant to suck. In 1877, a medical study of syphilis prevention described condoms as "the least bad system, and so much the better if a condom is more likely to inspire disgust than provoke desire. The number of couplings, and consequently of cases of [infection], will thereby be reduced." In other words, if condoms suck badly enough, maybe people will get so turned off that they won't have sex anymore.

Yeah, that's worked really well.

That mindset still exists today: Abstinence is touted as the best solution to sexually transmitted infections, and condoms are just a stopgap for the weak-willed. Although progressive thinkers don't believe that drivel, they haven't done much to change it.

Think of the problems we've solved in the last half-century alone — problems we didn't even know we had. The problem of not being able to carry your entire record collection in your pocket. The problem of not having a giant inflatable pillow pop out of your steering wheel in a crash. The problem of not having a video camera with you at all times. Why are more people not pissed off about the problem of how much condoms suck?

Go ahead, minimize the importance of that "little bit" of lost sensation all you want, but remember: On a daily basis, millions of people risk their health, and their lives, to bridge the pleasure gap inherent in condoms. Human beings are wired for sexual pleasure. To dismiss the critical nature of that pleasure is to dismiss the circuitry that ensures the survival of the species. Why sacrifice sexual pleasure on the altar of inertia? It's literally a matter of life and death.

There have been enormous benefits from antiretroviral therapy, including pre-exposure protection to HIV. Countless lives depend upon that, and we must continue efforts to develop an HIV-prevention vaccine, to implement widespread male circumcision, and to do everything we can to stop the spread of AIDS. But those efforts also must include putting a new, improved, kick-ass condom on the same biomedical fast track as the other stuff.

Feeling glad that you don't live in the days of leather condoms? Quit feeling smug and start imagining a future in which you feel grateful to have escaped the days of wired phones, compact discs and latex condoms. There's too much complacency around the suckiness of this Stone Age bullshit. Where is our Steve Jobs of condoms? Where is our visionary, who sees a way out of this rubber prison?

A few efforts at innovation have been made. The female condom never gained traction. A microbicidal gel known as the "invisible condom" has yet to become visible. A spray-on condom was abandoned due to technical difficulties. Apple tried to make a touch screen telephone but gave up because it was too difficult and unprofitable. No, wait — that last one didn't actually happen. The opposite did.

Until we chase the condom with the same fervor — and budget — as we did the race to the moon, we're ripping off the next 3 million people who will be diagnosed with HIV this year. The abstinence-only crowd will throw a hissy fit, of course, but fuck 'em. They were against safe sex in the first place, an idea that has saved, and will continue to save, lives. The next step is to demand a better alternative to the condom. We'll save countless more lives, and we'll feel good doing it.

Paul R. Abramson is a professor of psychology at UCLA and the author (with Steve Pinkerton) ofWith Pleasure: Thoughts on the Nature of Human Sexuality. L.J. Williamson is a regular contributor toL.A. Weekly.

UC Berkeley professor denies link between HIV and AIDS

2012-02-23T08:41:00.000-08:00

BY FRANKLIN KRBECHEK | STAFF

For over 20 years, UC Berkeley professor Peter Duesberg has believed that HIV does not cause AIDS, an opinion that he says has limited his academic career and alienated him from the scientific community.

“You cannot find the (HIV) virus, only antibodies, and it doesn’t spread via sex as it should,” Duesberg said. “HIV is a harmless virus. I have said that before, and I continue to say it.”

The tenured professor of molecular and cell biology — who said he has been called “homophobic” and a “mass murderer” in the past for his beliefs — elicited further controversy after the publication of his most recent article in a scientific journal sparked the resignation of a member of the journal’s editorial board.

Near the end of January, Klaudia Brix of Jacobs University in Germany resigned from the board of the Italian Journal of Anatomy and Embryology in protest of the December publication of Duesberg’s article, entitled “AIDS since 1984: No evidence for a new, viral epidemic — not even in Africa.”

“It’s just propaganda that they’re dying from AIDS,” Duesberg said.

The article compares statistical evidence of AIDS deaths in Uganda and South Africa to the overall population growth of those countries and sub-Saharan Africa as a whole. The article then concludes that AIDS has not caused a large number of deaths in Africa.

“We deduce from this demographic evidence that HIV is not a new killer virus,” the article states.

However, Arthur Reingold, professor of epidemiology and associate dean for research at the UC Berkeley School of Public Health, said that Duesberg’s beliefs run counter to a core tenet held by the medical community.

“The HIV virus is the cause of AIDS,” Reingold said. “It is a well-established scientific fact going back 30 years. Every credible scientist in the world believes that to be a scientific fact.”

Three years after the announcement of the discovery of the AIDS virus in 1984, Duesberg published an article denying that HIV is the cause of AIDS.

He has since argued that AIDS results from recreational drug use and has advised those with the disease not to take anti-retroviral drugs.

“I tell people, by all means, stop taking these drugs — they haven’t cured anybody yet,” Duesberg said.

But other AIDS researchers rebuke his arguments as the spread of misinformation.

“People who deny the causality of AIDS are denying reality,” said Jeff Sheehy, director for communications at the UC San Francisco AIDS Research Institute, in an email. “I know individuals infected with HIV who are dead because they believed denialists and … initiated treatment too late to save their lives.”

Although Duesberg’s research has largely been restricted to small journals, he has published over 20 articles, three of those in Science, and a book on the virus, according to his website.

Despite this exposure, Duesberg said his beliefs have limited his academic career on campus. He has been teaching a laboratory course since 1987 and claims he was restricted by other faculty from giving a lecture for more than 20 years.

“I never got to teach a course in my field until recently,” Duesberg said, referring to the lecturing position he was given in the fall semester of 2009. “My colleagues didn’t trust me.”

G. Steven Martin, chair of the campus department of molecular and cellular biology, declined to comment on Duesberg’s role in the department.

Despite overwhelming opposition, Duesberg does claim to have had some success in his research on AIDS.

“I get tons of letters saying ‘thank you, your research has changed my life,’” he said.

Going forward, Duesberg plans to pursue cancer research, lessening his focus on AIDS.

“You try to make your case as good you can, and I think I’ve done that,” he said. “I have said what I can say — I don’t think I can do too much more.”

Is an “HIV Prevention Pill” Worth It? - AHF SPEAK OUT

2012-02-23T07:09:00.000-08:00

In the United States, the Centers for Disease Control and the Federal Drug Administration (FDA) have expressed interest in establishing guidelines for the use of PrEP. Under the current regulations, a medical provider is allowed to prescribe ART to a HIV negative person. This is called ‘off-label use’ – use of an HIV/AIDS medication for purposes other than treatment of HIV— effectively constitutes PrEP. However, as long as PrEP is not officially sanctioned by the FDA, drug companies cannot market ARTs as a preventative measure to the public. If PrEP is eventually approved by the FDA, pharmaceutical companies stand to make a lot of money catering to a new market in the developed world instead of providing cheaper—and much needed—drugs in the developing world.

Internationally, PrEP has also received attention from the EU, the World Health Organization and various civil society organizations and advocates in the global health arena. The fact that PrEP is being considered as an evidence-based HIV prevention approach is incomprehensible at a time when the world cannot treat all people with HIV who are already ill.

With the continued assault on generic drug manufacturers by Big Pharma and a stagnating commitment by the rich countries to contribute more money to the global AIDS fight, PrEP looks more like a pharmaceutical cash cow in the making, than a viable or prudent public health initiative. In the United States, one year of ART can cost upwards of $10,000 USD. Currently, there are waiting lists in the US for HIV-positive low-income people in need of treatment. In Eastern Europe, Central Asia and Africa ART coverage remains unacceptably low and far behind the Universal Access target of 80% for all who need it. Is it possible to justify giving PrEP to healthy people while the sick and dying are waiting for treatment?

The legitimization of PrEP is detrimental because it could lead to a false sense of security among people who are currently using condoms to protect themselves. To achieve even a modest level of protection, PrEP requires strict adherence to a daily ART regimen. If we ponder that adherence to ART among HIV-positive patients still remains a challenge in many places and that side effects associated with ART can be severe, the likelihood of an HIV-negative person taking the medication consistently as a preventative measure seems low.

As long as there is no compelling scientific evidence proving that PrEP is effective, the global health community must focus on the things that do work. Global AIDS control lies in finding equilibrium between the prevention of new infections and treatment of people who need lifesaving medication. The HPTN 052 clinical trial proved that ART works as prevention, by lowering infectiousness in HIV positive people by 96%. Condoms, when consistently used have also been shown to be over 90% effective in preventing new infections.

When it comes to prevention of new HIV infections, condoms are by far more cost-effective and reliable than PrEP. However, the global health establishment has come upon numerous political, economic and ideological challenges in trying to promote condom use. Prevention work is tedious and difficult, as evidence by the continuingly growing number of new HIV infections in the world. Perhaps prevention is even more challenging then treatment, which may explain eagerness by some to embrace PrEP despite its questionable effectiveness. Unfortunately, when it comes to prevention there is no magic pill.

Denys Nazarov
Global Policy Coordinator

"Positively False" – HIV and AIDS Documentary - London Screening and Q & A

2012-02-22T09:17:00.000-08:00

Positively False – Birth of a Heresy. Joan Shenton reaches back to 1987 through her extensive archive of broadcast and non-broadcast video material on HIV and AIDS combining it with current footage.

In this documentary dissident scientists, journalists and activists are voicing their concerns about the way the infectious hypothesis for AIDS took over from the toxic one and highlights the impact the dogma surrounding a viral cause for AIDS has had on people’s lives. The film travels through Africa, Europe and the United States revealing the way plague terror, financial objectives and scientific skullduggery have led to tragic examples of toxicity and death from antiviral drugs, social stigma, broken families, fear of sex, homophobia and imprisonment. Positively False – Birth of a Heresy is produced by Meditel Productions Ltd andThe Immunity Resource Foundation in association with Yellow Productions.

What’s next for the HIV/AIDS vigilantes at Treatment Action Campaign?

2012-02-21T07:36:00.000-08:00

by Henry Bauer

Just a couple of months ago, I noted that the Treatment Action Campaign in South Africa had urged the Gates Foundation not to proceed with trials comparing stavudine to tenofovir because stavudine is so much more toxic and should simply be replaced by tenofovir forthwith. I noted too how strange this seemed, given that the toxicity of tenofovir is high and well known, as I had noted in several posts; see“HAART is toxic: Mainstream concedes it, in backhanded ways” (2011/12/30).
What will TAC do next, given that the toxicity of tenofovir is becoming talked about increasingly?

“In their analysis of comprehensive VA electronic health records, the study authors found that for each year of exposure to tenofovir, risk of protein in urine — a marker of kidney damage — rose 34 percent, risk of rapid decline in kidney function rose 11 percent and risk of developing chronic kidney disease (CKD) rose 33 percent. The risks remained after the researchers controlled for other kidney disease risk factors such as age, race, diabetes, hypertension, smoking and HIV-related factors. . . . Patients were tracked for an average of 1.2 years after they stopped taking tenofovir. They remained at elevated risk for at least six months to one year compared with those who never took the drug, suggesting that the damage is not quickly reversible . . . . ‘We do not know the long-term prognosis for these patients who stop tenofovir after developing kidney disease’”.
(Of course the authors of the reported study pointed out that HIV itself increases the risk of kidney damage. HIV itself is blamed by HIV/AIDS believers for every ill that antiretroviral drugs bring, for example “HIV-associated lipodystrophy”. Strange that all this supposed harm done by “HIV” was first noted only after antiretroviral drugs came into use.)

I confess that my query, what’s next for TAC, is replete with unashamed and undisguisableSchadenfreude.
The Treatment Action Campaign (TAC) in South Africa exemplifies as actively virulent a set of HIV/AIDS groupies and vigilantes as one could find anywhere. It is not too easy, though, to find out who exactly are the individuals who staff TAC. The website identifies only the “Leadership” of Vuyiseka Dubula, TAC General Secretary, and Nonkosi Khumalo, TAC Chairperson; and the Contact page gives the name only of the PR person (“Media Comment”), Caroline Nenguke. In this type of organization, these positions are figureheads, the real work being done by full-time staff.
The Annual Report for 2010 like the website gives no names of staff, not even who wrote the Report. It does mention — as had earlier news items — that funding has declined in a way that has made it necessary to retrench. Were I a donor, I would be unhappy at the Annual Report’s acknowledgement that the budget shows “General and Administrative” expenses at 21.7 million, not much below what was spent on “Programmes and Projects” at 27.6 million (currency is not indicated, presumably SA Rand). However, the Report does give a link for the full financial reports, and the 2011 one has the names of 5 directors: NAC Khumola, V Dubula-Majola, N Geffen, MJ Heywood, and TT Diamini, as well as two who had resigned in 2010: A Achmat and TGP Klaas. Compensation for the 5 directors is shown as 777,019 (if in South African Rand, a bit over US$100,000), a very small part of the 21,700,000 “General and Administrative” expenses. What were the other parts?
Nathan Geffen is a member of “AIDStruth.org”, co-authored Edwin Cameron’s book, “Witness to AIDS”, and himself has written “Debunking Delusions: The Inside Story of the Treatment Action Campaign” (2010). He is active not only in HIV/AIDS matters but also politically, active among Jews who are critical of Israeli policies and actions. Mark Heywood is Director of the AIDS Law Project, whose website is as lacking in individuals’ names as is the TAC website.
I am irrevocably suspicious of organizations that do not give up front the names of all their significant staff and that do not in public documents itemize expenditures on salaries and associated benefits, just as I’m not interested in the views of bloggers and commenters who hide their identities. When things are not revealed, it seems reasonable to infer that revealing those things would discredit whoever wants them to remain hidden.

Liam Scheff and Robert Scott Bell Health Freedom Expo HIV AIDS Promo

2012-02-16T12:34:00.000-08:00

HIV Tests Are Not HIV Tests. WHAT? part 2

2012-02-15T11:46:00.000-08:00

Exploring more from the posting HIV Tests Are Not HIV Tests. WHAT? dated FEBRUARY 7, 2012. Henry H. Bauer, Ph.D. adds:

Abstract

HIV tests do not detect HIV. The seminal papers did not demonstrate HIV to be the cause of AIDS. The patent based on this work did not demonstrate that HIV tests are specific for HIV. The progression from “HIV is the probable cause of AIDS” to “HIV antibodies demonstrate active infection by HIV” came by assertion and not evidence. HIV-test-kits do not claim that the test detect infection, and they have never been approved for that purpose. There is no gold standard for an HIV test, and the existing tests are at best adjuncts to clinical diagnosis.

Drastic consequences include that healthy individuals are subjected to iatrogenic harm through life-long intake of highly toxic medication.

Introduction

So-called “HIV tests” do not detect infection by HIV (human immunodeficiency virus, a retrovirus), even though for more than a quarter century these tests have been widely used precisely as purported diagnosis of such infection. The manufacturers of the test kits do not claim that the tests detect infection, nor has the Food and Drug Administration approved the tests for that purpose, and authoritative discussions of how to detect HIV infection make plain that the tests are insufficient to diagnose infection.

The story behind this circumstance has a number of parts:

1. The initial claimed discovery or identification of a retroviral cause of AIDS.

2. The patented method for detecting antibodies claimed to be specific to human immunodeficiency virus.

3. A progression from claiming to find antibodies to presuming that presence of antibodies signifies active infection --- without the benefit of any specific evidence to that effect and in the face of evidence to the contrary.

4. In absence of any gold standard test, the first (unproven, unvalidated) antibody test has been the basis for supposed validation of all later tests.

The consequences of the mistaken equating of “HIV-positive” with “infected by human immunodeficiency virus” could not be more serious. Healthy individuals who happen at some time to test “HIV-positive” have suffered physical, psychological or financial damage as a result of such a “diagnosis”; particularly harmed have been gay men and people of African ancestry.

In the following, when citing early work that employed the nomenclature of HTLV-III and LAV, those terms are used rather than the now-agreed term “HIV.”

ANNOUNCEMENT of an AIDS-causing retrovirus

HTLV-III was the probable cause of AIDS, the Secretary for Health and Human Services announced on 25 April 1984 at a press conference, introducing the purported discoverer, Robert Gallo. Four later publications in Science repeated that claim.

Popovic et al. ¹ described an immortalized T-cell line in which large quantities of HTLV-III could be obtained by co-culture with putatively infected T-cells. Retrovirus was detected through the presence of “particle-associated RT [reverse transcriptase]”, and RT activity was also the criterion for choosing a sucrose density of 1.16 g/ml as the “band” in which retrovirus would be found under ultracentrifugation. However, reverse transcriptase activity is present in normal cells, which vitiates a central element in this work as well as in much subsequent research on HIV: the “particles” with which RT activity was associated could just as well have been cellular debris and not virions. Electron microscopy claiming the presence of large amounts of “extracellular viral particles” was not supported by evidence that these particles were in fact virions. The virus was also said to be detectable via antigen-antibody reaction, but this involved a tautology, see in the next section “Isolation is not isolation; purification is not purification.”

It was further stated that HTLV-III proteins had been found in 85% of sera from AIDS patients and that HTLV-III is related to HTLV-I and -II, retroviruses previously discovered by Gallo, whereas by contrast the lymphadenopathy-associated retrovirus LAV described earlier by Barré-Sinoussi and Montagnier was not related to HTLV-I or -II and was reactive to only 37.5% of sera from AIDS patients. Those claims were soon shown to be false. HTLV-III in fact was LAV, a sample of which Montagnier had sent to Gallo; and the 2009 Nobel Prize for discovering the virus went to Barré-Sinoussi and Montagnier to the exclusion of Gallo. Numerous flaws have been uncovered in the work reported from Gallo’s laboratory, and it was owing only to a technicality that Gallo himself failed to be charged formally with scientific misconduct ².

In an article immediately following that of Popovic et al. ¹, Gallo et al. ³ claimed to have isolated HTLV-III from 26 of 72 AIDS patients, 18 of 21 individuals with pre-AIDS, 3 of 4 healthy mothers of children with AIDS, and 1 of 22 “normal male homosexual subjects.” However, as an illness becomes more severe, one might expect to find more of the pathogenic agent at work rather than less, so it seems strange that “the primary cause of AIDS” could be found in only 36% of those suffering from the active disease when it could be found in 86% of those merely with pre-AIDS. Moreover, the symptoms of “pre-AIDS” were fever and chronically swollen lymph nodes, seen in many illnesses and not specifically precursors to AIDS; those symptoms were presumed to be such precursors only when encountered in people belonging to the groups in which AIDS had appeared, gay men or injecting drug abusers. Beyond that, “isolated” is drastically misleading, see “Isolation is not isolation; purification is not purification” in the next section.

The third article published at the same time ⁴ again asserted that HTLV-III is “a true member of the HTLV family” yet “clearly distinguishable from HTLV-I and -II.” There were somewhat confused claims about which antigens are associated with which of these retroviruses. Thus p61 and p65 are “encoded by HTLV-I” yet often recognized by sera from AIDS patients. Antigens of HTLV-III are “similar in size” to those of other HTLVs but include three “serologically unrelated” groups: p55 and p24 which are “group-specific”; p65 is “envelope-related”; and the third group is “of unknown affiliation.” In one place it is said that “antibodies to the structural proteins of HTLV, notably p24 and p19 (15), are not detectable in most AIDS patients (16)”, yet later p24 is included among the “most prominent . . . antigens” of HTLV-III, namely p65, p60, p55, p41, p24; less prominent were said to be p88, p80, p39. p32, p28, p21. Some cross-reaction of p65 with HTLV-I was acknowledged, as well as cross-reactions with unspecific gag-related antigens. Nevertheless, specificity was claimed for p65, p55, p41, p39, p32, p24 as “newly expressed after viral infection”; but of course this does not preclude the possibility that these antigens might be found also in association with other agents than HTLV-III. It is pertinent that the immunological abnormalities seen in AIDS patients are also present in people suffering from, for instance, tuberculosis, diabetes, malaria, macroglobulinemia, aplastic anaemia, or thalassaemia, and that they can be induced by (for example) adrenalin, prednisone, or Epstein-Barr virus ⁵.

The fourth article ⁶ reported antigens of HTLV-III to be reactive with sera of 88% of AIDS patients and 79% of gay men with pre-AIDS symptoms as well as with under 1% of “heterosexual subjects.” This time the major reactivity was said to be against p41, a presumed viral-envelope antigen.

These papers fall far short of demonstrating that HTLV-III is a necessary and sufficient cause of AIDS. That has often been remarked, for example, “the evidence does not constitute proof of the isolation of a retrovirus, that the virus is exogenous or that the virus is causally related to AIDS” ⁷. All that the Gallo opus showed is that antibodies in sera from AIDS and pre-AIDS subjects react with material obtained from cultures infected with agents present in sera from AIDS and pre-AIDS subjects, a circular procedure ⁸ that does not clarify the nature of the “isolated” materials; nor had it been shown that similar reactivity is not present in other physiological conditions or in other illnesses than AIDS.

PAtent for detecting the virus

U.S. Patent 4,520,113 granted to Robert Gallo and co-workers Mikulas Popovic and Mangalasseril G. Sarngadharan, dated 28 May 1985, claims that “antigens associated with the infection of human cells by this virus are specifically recognized by antibodies from AIDS patients. Specifically, HTLV-III isolated from AIDS patients and transmitted by cocultivation with an HT cell line is specifically detected by antibodies from human sera taken from AIDS patients.”

Claimed test is non-specific

This nascent test was hardly foolproof, since sera from only 88% of AIDS patients and from 79% of pre-AIDS gay men showed positive and since positive reactions were also seen in some presumably uninfected blood donors ⁶. From the very beginning, the test was anything but specific.

One reason may be the claim of p41 as the most characteristic and prominent HIV-specific antigen, and that p65, p60, p55, and p24 too were “not detected in normal sera.” However, antibodies to p24 are found in substantial proportions of patients with multiple sclerosis, T-cell lymphoma, and generalized warts ⁹. Moreover, in about 15% of healthy blood donors, p24 was “the predominant band” on Western Blot tests, and p41 has also been found in blood platelets of healthy individuals ⁷. Far from being specific to HIV or AIDS patients, then, p24 and p41 are not even specific to illness.

Isolation is not isolation; purification is not purification

In the patent as well as in the earlier articles in Science, and in the HIV/AIDS literature overall to date, “isolation” and “purification” do not have the meaning those terms convey in common parlance or when used by chemists or physicists. For the latter scientists and for most people, isolation means to extract solely the pertinent entity free from all other material. Purification means, similarly but not identically, to remove all contaminants to leave only the pertinent entity.

In HIV/AIDS parlance, however, “isolation” and “purification” do not mean getting pure HIV from an AIDS patient: that has never been shown to be done in the only possible way, which would be to detect by electron microscopy actual virions of HIV and nothing else in a purified sample taken directly from a patient. Instead, HIV “isolation” means that serum from a patient is cultured together with various cells and reagents and that a later extract from that culture reacts “HIV-positive.” It is assumed that the culturing amplifies already-present HIV, but one cannot exclude that the culturing actually produced ab initio whatever was generating a positive test-response. Indeed, human genomes include some DNA sequences homologous with “HIV”, and these may be expressed by culturing techniques like those used in HIV/AIDS research ⁷.

“Purification” in HIV/AIDS parlance means that material thought to contain HIV is ultracentrifuged in a specified medium, and what sediments at a particular density is regarded as “HIV.” In point of fact, published electron micrographs of such “purified” “isolates” show a motley mixture of cellular debris, by far not pure virions ¹⁰.

Gallo has even asserted that there is no need to purify HIV since his method of culturing produces so much of it that it did not matter what else might have been present:

You have to purify. . . . [A] retrovirus comes out of chromosome membrane. In so doing, it incorporates some cellular proteins in the virus. . . . [B]y putting it through a sucrose gradient it would do hardly anything when you have very little virus. So the ratio of cellular material to virus, I don’t want to say this is an accurate number but I will give an example. Let’s say it would be a thousand to one but when we succeeded in mass producing the virus in a continuous culture, you have got an enormous purification far beyond the sucrose gradient alone because you are now producing loads of virus with little amounts of cell. ¹¹

It is far from obvious why each virion would incorporate less cellular protein in mass culture, but in any case the presence of even tiny amounts of some unknown, undetected, active agent can confound experiments. There can be no substitute for complete purification, literal isolation.

No longer operative

A number of assertions in the patent have since been quietly forgotten, for example that there is a certain cross-reactivity with Gallo’s HTLV-I and HTLV-II retroviruses. Gallo had earlier reported isolation of HTLV-I from an AIDS patient ¹² and described HTLV-I and -II as “the only known specific co-factors for AIDS” (emphasis in the original) ¹³.

The patent assigns the main specificity of the test to p41, with some reactivity also to p65, p60, p55, and p24. But the contemporary criteria for Western Blot tests call for any 1 or 2 of p160, p120, p41, not necessarily the “most prominent” p41; and some 2 or 3 among p68, p55, p53, p39, p32, p24, p18. Only 3 of the 5 antigens said by Gallo to be specific for HIV are among the 10 now supposedly Western-Blot specific for HIV ¹⁴.

Arbitrary criterion for “positive”

The primary antibody test (ELISA) measures a color intensity. Controls are not perfectly colorless, however; what intensity of color shall be judged “positive”?

The patent’s Example 1 reports that “absorbance readings greater than three times the average of 4 normal negative control readings were taken as positive.” Under that criterion, 88% of AIDS patients, 79% of pre-AIDS individuals, 60% of intravenous drug abusers, and 27% of gay men tested positive; 0.5% of controls also tested positive. That is hardly foolproof, specific detection of whatever might be uniquely characteristic of AIDS.

In other ways, too, the patent is less than impressive. Example 1 and Example 4 both refer to the data in Table 1 and describe the same procedure, though in somewhat different words; why they are given as distinct separate examples is puzzling. In a single paragraph, Example 5 asserts a finding of specificity without stating how many experiments were carried out.

Not an HIV test

In effect, the manner in which this test was developed makes it at best an AIDS and pre-AIDS test, not an HIV test, and more sensitive to and specific for pre-AIDS and not AIDS. Moreover, since the symptoms of pre-AIDS --- swollen lymph nodes, fever --- are seen also in many other illnesses, the test is nothing more than a nonspecific illness test. That is why over the years the Centers for Disease Control and Prevention (CDC) added dozens more illnesses to the list of “AIDS” diseases: patients with many illnesses may react “HIV-positive.”

antibodies as denoting infection

The scientific publications and the patent claiming HTLV-III to be the probable cause of AIDS were clearly insufficient to establish the claim. How then did it come about that a less-than-specific antibody test became a basis for asserting actual infection by HIV?

Rodney Richards, who worked on the development of the first ELISA HIV test (marketed by Abbott Laboratories), has described in chronological detail how this unprecedented equating of antibodies with active infection came about ¹⁵. The story would be literally incredible were it not fully documented by authoritative material in the public domain.

Initially, in 1984, the CDC had quite properly acknowledged the possibility of false-positive antibody tests owing to “an antigenically related virus or nonspecific test factors.” In people at high risk of AIDS, it “probably” meant prior exposure, however, “Whether the person is currently infected or immune is not known . . . . the frequency of virus in antibody-positive persons is yet to be determined” ¹⁶.

Six months later, CDC admitted that there would be a high proportion of false positives when screening low-risk populations: no one should be informed of testing positive before the test had been duplicated ¹⁷.

Three months beyond that, the Food and Drug Administration approved Abbott’s ELISA test for blood screening. Obviously it makes sense to take all possible precautions against the presence of a possible pathogen in blood that is to be used for transfusions: better to discard 100 donations of good blood than to allow 1 infected sample to be transfused. It is very different, however, to inform someone on the basis of a highly unreliable test that they are infected with a deadly pathogen for which there is no cure. The package insert with the Abbott test had the appropriate caveats: “there is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood. . . . The risk of an asymptomatic person with a repeatedly reactive serum sample developing AIDS or an AIDS-related condition is not known.” The same caveats apply to the Western Blot antibody-test approved in 1987 and widely used as supposed confirmation of duplicate positive ELISA tests ^{15, p.339}. Similar disclaimers from various manufacturers are found in more recent test-kit inserts ¹⁸.

Some months after the Abbott test had been approved for blood screening, data from blood donors revealed that 44% of samples strongly positive for “HIV” antibody contained no virus detectable by culture. Similarly, 40% of gay men testing antibody-positive had no detectable virus ¹⁹. In nearly half of all cases, then, both in a high-risk group and in a low-risk group, a positive “HIV” test came in absence of HIV.

Then CDC stood this evidence on its head. The data showed that absence of virus accompanied antibody-positive in almost half of all cases. Looking instead at the other half, CDC asserted that “Since a large proportion of seropositive asymptomatic persons have been shown to be viremic (5), all seropositive individuals, whether symptomatic or not, must be presumed capable of transmitting this infection” ²⁰ [reference (5) ¹⁷ admitted that it was not known what proportion of seropositive donors was actually infected].

Perhaps CDC was so concerned to prevent transmission of HIV that it used the same reasoning as with blood screening: better that some large number of actually non-infected people be warned against passing on a possibly fatal infection than that a small number of infected persons unwittingly infect others. But that ignores the devastating psychological effect on the many uninfected people who were thereby doomed to believe that they were harboring an incurable, inevitably fatal infection.

CDC then went even further than “presuming” that seropositive might mean infection: in 1986, in an article in the journal of the American Medical Association --- much more widely read than the Mortality and Morbidity Reports in which the “presumption” had been stated --- CDC researchers defined seropositive as equivalent to infection ²¹. As Richards points out ¹⁵, all the cited data reported that virus could not be cultured from a high proportion of seropositive individuals. By asserting that seropositive equals infection, CDC was dismissing evidence from culture, implying that there was something ineffective in the virus-culturing procedure and substituting for that a test which had never been validated.

CDC has continued to dispense with all caveats, asserting that “presence of antibody indicates current infection” ²²: not as a precautionary measure in screening blood, not as a precautionary measure to prevent transmission, not when the seropositive individuals are in a high-risk rather than low-risk population, and irrespective of whether they are symptomatic or asymptomatic; it is asserted dogmatically without any exception that seropositive means infected. Surely this constitutes public-health malpractice based on junk science.

Furthermore, Richards ¹⁵ points out that CDC was actually transgressing its mission to safeguard public health by this assertion which dictates what doctors should do on the basis of a particular test, even in the face of what the Food and Drug Administration, charged with protecting consumers, had said just a few months earlier: “The significance of antibodies in an asymptomatic individual is not known” ²³.

Some twenty years later, it is clear that the CDC’s dogmatic insistence that “HIV-positive” equals infection has resulted in widespread iatrogenic harm, in many cases death, through the administering of toxic antiretroviral drugs to uninfected individuals.

NO gold standard for HIV tests

The work just reviewed dates from the 1980s. Were the deficiencies corrected by later work?

Unequivocally and simply, “No.”

For one thing, all later work has built on and presumed the soundness of the seminal articles. For another, it remains understood by the actual experts that a positive “HIV” test does not in itself signify infection, be the test an ELISA, a Western Blot, a “viral load” measurement, or a culture; but this understanding is not broadcast outside the technical literature.

The following is taken from Weiss and Cowan ²⁴, which can be regarded as authoritative on several grounds: Weiss has worked in this field since the beginning, having published since 1984 including with Gallo; and this is a chapter in the fourth edition (2004) of a monograph that has been favorably accepted and reviewed (e.g. the 3rd edition in JAMA ²⁵ and the 4^th in Clinical Infectious Diseases ²⁶ or JAMA ²⁷).

In terms of substance, really no more need be said than that

In the absence of gold standards, the true sensitivity and specificity for the detection of HIV antibodies remain somewhat imprecise (p. 150).

Obviously enough, “somewhat imprecise” is a euphemism: the lack of gold standard makes everything highly doubtful. Pure virions of HIV, the sine qua non for establishing a veritable gold standard, have never been obtained from an AIDS patient or from an “HIV-positive” individual. Twenty-five years of HIV/AIDS research have not brought unequivocally valid HIV tests.

Weiss and Cowan make clear that inferring HIV infection is a matter of probability, not certainty, and that the assessment of probability requires interplay of laboratory testing with clinical information, very much including individual medical history and risk-category classification:

A pre-test probability assessment is required whenever test results are to be meaningfully interpreted (p. 149; emphasis in original)

An essential part of the testing process takes place even before testing is done; that is, the estimation of the probability of infection (the ‘pre-test’ probability). This is necessary in order to interpret a test result appropriately, whatever the purpose --- whether it is clinical, counseling or research --- and can dramatically impact the predictive value after testing (or ‘post-test’ probability) (p. 159)

No test, per se, should be the basis for diagnosis on its own, but rather a test is merely an aid in correct diagnosis. The practitioner must use test results in the context of a clinical picture to reach an accurate diagnosis (p. 172)

The import of these uncertainties is illustrated in a table ^{24, p.149} showing that in low-risk populations (prevalence of “HIV” 0.1%), a “positive” “HIV”-test-result has only about 1 chance in 6 of being a “true” positive; 5 out of 6 would be false positives. Conversely, at a prevalence of 99.9%, a negative test-result would have only about 1 chance in 6 of truly being negative --- once an individual has been designated “high risk”, even a negative “HIV” test may not be accepted as definitively showing lack of infection, further testing is recommended.

This illustration is based on a hypothetical test that is 99.5% sensitive and 99.5% specific, but the principal point is independent of the actual numbers --- and no test, of course, is 100% sensitive or specific. Thus the initial belief that a person is high or low risk biases interpretation of the laboratory tests to becoming self-fulfilling prophesies.

Conclusions

There is no gold standard for HIV tests. Positive tests do not prove infection by HIV. Nevertheless, current practice is to take positive tests as proof of active infection. As a result, healthy people are unwarrantedly doomed to lifelong administration of toxic drugs. This applies particularly to people in groups traditionally regarded as “high risk”: gay men and injecting drug users; but in recent years African Americans have come to be regarded as being at high risk, and positive tests are also common among TB patients and as a result of pregnancy. Only the slightest indication of ill health --- or indeed just routine “HIV” testing --- suffices for individuals in any of those groups to be told they are infected and are then assigned to antiretroviral treatment .

Acknowledgments

I am very grateful to Rodney Richards for clarifying discussions, particularly the crucial insight that the “HIV” test was really an AIDS test.

_______________________________________________________________________

FOOTNOTE:
Henry H. Bauer, Ph.D., is Professor Emeritus of Chemistry & Science Studies and Dean Emeritus of Arts & Sciences at the Virginia Polytechnic Institute & State University (Virginia Tech).

1306 Highland Circle, Blacksburg VA 24060-5623. E-mail: hhbauer@vt.edu

________________________________________________________________________

POtential COnflict of Interest

I am the author of the book, The Origins, Persistence and Failings of HIV/AIDS Theory, which claims to show that HIV is not the cause of AIDS.

References

¹ Popovic M, Sarngadharan MG, Read E, Gallo RC. Detection, isolation, and continuous production of cytopathic retroviruses (FLV-F) from patients with AIDS and pre-AIDS. Science 1984;224:497-500.

² Crewdson J. Science Fictions: A Scientific Mystery, a Massive Coverup, and the Dark Legacy of Robert Gallo. Boston etc.: Little, Brown; 2002.

³ Gallo RC, Salahuddin SZ, Popovic M, et al. Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at Risk for AIDS. Science 1984;224:500-503.

⁴ Schupbach J, Popovic M, Gilden RV, et al. Serological analysis of a subgroup of human T-lymphotropic retroviruses (HTLV-III) associated with AIDS. Science 1984;224:503-505.

⁵ Papadopulos-Eleopulos E. Reappraisal of AIDS: Is the oxidation induced by the risk factors the primary cause? Medical Hypotheses 1988;#25:151-162.

⁶ Sarngadharan MG, Popovic M, Bruch L, et al. Antibodies reactive with human T-lymphotropic retroviruses (HTLV-III) in the serum of patients with AIDS. Science 1984;224:506-508.

⁷ Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM. Has Gallo proven the role of HIV in AIDS? Emergency Medicine [Australia] 1993;5:113-123.

⁸ Hodgkinson N. Why an HIV test may not provide proof positive at all. The Business, May 9/10, 2004:1,6; HIV diagnosis: a ludicrous case of circular reasoning. ibid., May 16/17, 2004:1,4.

⁹ Ranki A, Johansson E, Krohn K. Interpretation of antibodies reacting solely with human retroviral core proteins. N Engl J Med 1988;318:448-449.

¹⁰ Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations. Virology 1997;230:125-133; Bess JW, Gorelick RJ, Bosche WJ, et al. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. ibid. 134-144.

¹¹ Transcript of Gallo testimony is available at http://garlan.org/Cases/Parenzee/Gallo.html. Accessed 27 November 2009.

¹² Gallo RC, Sarin PS, Gelmann EP, et al. Isolation of human T-cell leukemia virus in Acquired Immune Deficiency Syndrome (AIDS). Science 1983;220:865-867.

¹³ Gallo RC. Virus Hunting: AIDS, Cancer, and the Human Retrovirus. New York: BasicBooks; 1991; p.248.

¹⁴ Papadopulos-Eleopulos E, Turner VF, Papadimitriou JM, et al. Mother to Child Transmission of HIV and its Prevention with AZT and Nevirapine. Perth, Western Australia: The Perth Group; 2001. Available at http://www.theperthgroup.com/monograph.html. Accessed 27 November 2009.

¹⁵ Richards R. The birth of antibodies equals infection. App. II, pp. 333-340 in Farber C. Serious Adverse Events: An Uncensored History of AIDS. Hoboken NJ: Melville House; 2006.

¹⁶ Antibodies to a retrovirus etiologically associated with Acquired Immunodeficiency Syndrome (AIDS) in populations with increased incidences of the syndrome. Morb Mortal Wkly Rep, July 13, 1984;33:377-379.

¹⁷ Provisional Public Health Service inter-agency recommendations for screening donated blood and plasma for antibody to the virus causing Acquired Immunodeficiency Syndrome. Morb Mortal Wkly Rep, January 11, 1985;34:1-5.

¹⁸ Zip file of test-kit inserts, aras.ab.ca/HIVTestInformation.zip. Accessed 27 November 2009.

¹⁹ Current trends update: Public Health Service Workshop on Human T-Lymphotropic Virus Type III antibody testing --- United States. Morb Mortal Wkly Rep, August 9, 1985;34:477-478.

²⁰ Current trends: Additional recommendations to reduce sexual and drug abuse-related transmission of Human T-Lymphotropic Virus Type III/ Lymphadenopathy-Associated Virus. Morb Mortal Wkly Rep, March 14, 1986;35:152-155.

²¹ Ward JW, Grindon AJ, Feorino PM, et al. Laboratory and epidemiologic evaluation of an enzyme immunoassay for antibodies to HTLV-III. JAMA 1986;256:357-361.

²² Perspectives in disease prevention and health promotion. Public Health Service guidelines for counseling and antibody testing to prevent HIV infection and AIDS. Morb Mortal Wkly Rep, August 14, 1987;36:509-515.

²³ Cruzan S. FDA News, April 30, 1987:p.87-11; cited in Richards ^xv.

²⁴ Weiss SH, Cowan EP. Laboratory detection of human retroviral infection. Chapter 8 in Wormser GP (ed.). AIDS and Other Manifestations of HIV Infection. London etc.: Academic Press; 2004 (4th ed.).

²⁵ Panwalker AP. JAMA 1999;281:1757.

²⁶ Johnson SC. Clin Inf Dis 2005;40:1866-1867.

²⁷ Manfredi R. JAMA 2005;293:1393-1394.

Conflicting data on bone fracture link to HIV meds

2012-02-14T11:13:00.000-08:00

The EATG
Whether specific drugs such as tenofovir increase the risk, reduce the risk, or have a variable effect over time remains unclear.

Overall, use of antiretroviral therapy (ART) appears to be associated with a decreased likelihood of bone fractures among people with HIV, but whether specific drugs such as tenofovir increase the risk, reduce the risk, or have a variable effect over time remains unclear based on conflicting data reported in the February 1, 2012, advance online edition of AIDS.

Numerous studies over the course of the epidemic have found that HIV positive people are more likely to have low bone mineral density (BMD) and bone loss (osteopenia, or the more severe osteoporosis) compared with the general population. It is not clear whether this is related to HIV itself, inflammatory or metabolic changes associated with chronic viral infection, effects of antiretroviral therapy, or some combination of factors -- nor is it certain whether low bone density actually leads to greater incidence of fractures.

ART Reduces Risk

In the first analysis, Linda Mundy from GlaxoSmithKline and colleagues assessed the risk for fractures associated with time-dependent exposure to different antiretroviral drugs.

This retrospective nested case-control study looked at a cohort of 59,594 insured HIV patients enrolled in medical care between January 1997 and March 2008, identified in the Ingenix Impact National Benchmark Database. A majority were men and the average age was about 40 years.

A total of 2411 case patients who had sustained fractures were each matched 4-to-1 with 9144 HIV positive control subjects without fractures. The researchers then analyzed differences in antiretroviral drug use between the case and control groups.

Results

Exposure to antiretroviral therapy overall was associated with significantly reduced risk of bone fractures (odds ratio [OR] 0.64).
Use of nucleoside/nucleotide reverse transcriptase inhibitor (NRTI) and non-nucleoside reverse transcriptase inhibitor (NNRTI) drug classes was associated with reduced fracture risk.
Exposure to protease inhibitors (PIs) was associated with a "null effect" that became slightly reduced among people with the longest duration of exposure (> 18 months).
Use of darunavir (Prezista), delavirdine (Rescriptor), and saquinavir (Invirase or Fortovase) were associated with increased fracture risk over time.
Efavirenz (Sustiva), emtricitabine (Emtriva), lamivudine (3TC; Epivir), tenofovir (Viread), and zidovudine (AZT; Retrovir) were associated with reduced fracture risk.
Abacavir (Ziagen), didanosine (ddI; Videx), nelfinavir (Viracept), ritonavir (Norvir), and stavudine (d4T; Zerit) were initially associated with increased risk, but this became null with longer duration of use.
Nevirapine (Viramune) was initially associated with a null risk that became reduced risk with longer use.
Amprenavir (Agenerase), atazanavir (Reyataz), enfuvirtide (T-20; Fuzeon), fosamprenavir (Lexiva), indinavir (Crixivan), lopinavir/ritonavir (Norvir), tipranavir (Aptivus), and zalcitabine (ddC; Hivid) were all associated with null or uncertain fracture risk.
Other significant fracture risk factors included history of prior fractures, heavy alcohol use, low physical activity, and low body weight.

"Our findings suggest an overall reduced risk for facture in persons treated versus not treated with antiretroviral drugs for HIV infection," the study authors concluded.

"For darunavir, although the number of fracture events were low, the estimate of risk was substantial...and further assessment of this PI in other study populations seems justified," they added in their discussion (adjusted OR 1.93, or about twice the risk).

With regards to tenofovir -- the drug most frequently linked to bone loss among people with HIV -- they wrote, "our time-censored subset analysis of abacavir versus tenofovir exposures revealed null risk in adjusted models for known risk variables and other antiretroviral drug exposures." Prior studies have seen larger reductions in bone density with tenofovir compared to abacavir, they noted, but have not found significant difference in the risk of non-traumatic fractures (breaks not due to traumatic injury).

As to why ART might reduce fracture risk, the authors explained that as BMD decreases with age, "the mechanisms of bone modeling are not unidirectional and untreated HIV infection has been associated with uncoupled bone formation and bone resorption that seems attributed to both viral and inflammatory effects."

Some Drugs Raise Risk

The second study in the same issue, however, contradicted some of Mundy's findings.

In this retrospective analysis, Roger Bedimo from the VA North Texas Health Care System and colleagues looked at the link between osteoporotic fractures of the wrist, vertebrae, or hip -- that is, breaks due to bone fragility rather than trauma -- among 56,660 HIV positive participants in the Veterans Affairs Clinical Case Registry between 1988 and 2009.

The researchers used 2 multivariate models: Model MV1 controlled for race, age, tobacco use, diabetes, body mass index, and hepatitis C status, while model MV2 controlled for the same variables plus antiretroviral drug exposure.

Results

Here, tenofovir exposure was associated with a small but significant increase in fracture risk in a univariate analysis (hazard ratio [HR] 1.08; P < 0.001), falling to 1.06 in both multivariate models.
Among 32, 439 patients who entered the cohort during the highly active antiretroviral therapy (HAART) era starting in the mid-1990s, tenofovir was associated with a yearly hazard ratio of 1.16 in a univariate analysis (P < 0.001), 1.13 in model MV1 (P = 0.001), and 1.12 in model MV2 (P = 0.011).
Boosted protease inhibitor exposure was also associated with a small increase in fracture risk: HR 1.11 (P = 0.001) in a univariate analysis, 1.08 (P = 0.026) in model MV1, and 1.05 (non-significant) in model MV2.
Within this class, lopinavir/ritonavir had an HR of 1.09, which was borderline significant (P = 0.051) in model MV2.
Osteoporotic fractures were also independently associated with older age, non-black race, low body mass index, and smoking.

Based on these findings, the researchers concluded, "Cumulative exposure to [tenofovir] and, among PIs, [lopinavir/ritonavir] were independently predictive of increased risk of osteoporotic fracture in the HAART era."

"Using a cohort of 56,660 HIV-infected patients followed for a mean of 5.4 patient-years, we found for the first time that exposure to [tenofovir]and [ritonavir-boosted protease inhibitors] were associated with a modestly increased osteoporotic fracturerisk," they wrote in their discussion. "After controlling for traditional osteoporotic fracturerisk factors, these associations were no longer statistically significant."

However, they continued, "stronger associations between either [tenofovir]or [ritonavir-boosted protease inhibitors] with osteoporotic fracture were found when analysis was limited to patients who entered the cohort in the HAART era...[Tenofovir] remained independently predictive of osteoporotic fracture risk (12% higher risk per year of exposure) after controlling for traditional osteoporotic fracture risk factors and concomitant [antiretrovirals] used."

Furthermore, they noted, "we found evidence of an interaction between [tenofovir] and [ritonavir-boosted protease inhibitors]...Concomitant exposure to both [tenofovir] and [ritonavir-boosted protease inhibitors] [was] associated with a greater osteoporotic fracturerisk than exposure to either [tenofovir] without [ritonavir-boosted protease inhibitors], or [ritonavir-boosted protease inhibitors] without [tenofovir]."

"These findings, if confirmed, might warrant consideration of osteoporotic fracturerisk in decisions [about] ART initiation among HIV-infected patients," they suggested, but emphasized that traditional -- and in some cases controllable -- risk factors such as low body weight and smoking are "much more important in predicting fracture risk among HIV-infected patients than antiretroviral exposure."

Further studies are needed to resolve contradictory findings about the impact of ART on bone health, and -- perhaps more important -- whether lifestyle changes or therapies such as vitamin D or biphosphonates drugs might help prevent bone loss and fractures among people with HIV.

By Liz Highleyman

References

LM Mundy, AO Youk, G McComsey, and SJ Bowlin. Overall benefit of antiretroviral treatment on the risk of fracture in HIV: nested casecontrol analysis in a health-insured population. AIDS. February 1, 2012 (Epub ahead of print).

R Bedimo, NM Maalouf, S Zhang, H Drechsler, and P Tebas. Osteoporoticfracture risk associated with cumulative exposure to tenofovir and other antiretroviral agents. AIDS. February 1, 2012 (Epub ahead of print).

HIVandHepatitis.com

http://hivandhepatitis.com/

http://hivandhepatitis.com/hiv-related-conditions/hiv-bone-loss-osteoporosis/3452-conflicting-data-on-bone-fracture-link-to-hiv-meds

ESPN to Show Film About Magic Johnson’s H.I.V. Disclosure

2012-02-14T07:01:00.000-08:00

When Magic Johnson (read a love letter to Magic Johnson) revealed on Nov. 7, 1991, that he had contracted H.I.V., the stunning announcement rippled across the National Basketball Association and professional sports, and changed the way that H.I.V./AIDS was discussed. Now, more than 20 years later, ESPN and the N.B.A. are preparing a documentary about Mr. Johnson’s decision to go public with his diagnosis, from a director who says that he doesn’t want to see H.I.V./AIDS disappear from the national conversation.

Dr. Nancy Padian 10-year study on HIV transmission

You want to know how Magic Johnson knows today? ask Bill Plaschke LA Times reporter

"It's exercise and faith and three pills twice a day. "

I beg him to give me the name of the three pills. He says everyone asks, but his doctors have sworn him to silence for the sake of those who might try to use those three pills to self-medicate.

What the REAL reason he won't answer this question?

On Friday ESPN Films and NBA Entertainment are expected to announce that they will present the documentary, called “The Announcement,” on ESPN starting on March 11. It is directed by the filmmaker and writer Nelson George. (Mr. George has been a contributor to The New York Times.)

Luc Montagnier, HIV discoverer, Nobel Prize Winnersays HIV Can Be Cleared Naturally

Mr. Johnson, who stepped down as point guard of the Los Angeles Lakers after making the announcement (he had a brief comeback in 1996), played on five N.B.A. championship teams, was named the league’s Most Valuable Player three times and was a 12-time All-Star. The film will include new interviews as he discusses the events that led up to his news conference. Also appearing in the film are Mr. Johnson’s wife, Cookie; his fellow Lakers James Worthy and Kurt Rambis and the team’s former general manager Jerry West; and Larry Bird, the Boston Celtics forward who was his athletic rival and is an off-court friend.

Mr. George said in a telephone interview that his goal for “The Announcement” was not only to tell the inside story of Mr. Johnson’s personal deliberations but also to “make people aware this thing hasn’t disappeared.” He added: “People are still dying of the virus. People are living very tough lives because of it. It’s falling off the national agenda, I believe, and this in some way helps us reintroduce it.”

Craig Fujii/Associated PressMagic Johnson on Nov. 7, 1991, announcing that he had tested positive for the virus that causes AIDS.

Mr. George said his memories of Mr. Johnson’s announcement were vivid and specific. He said the event was “for a lot of people of a certain age” the equivalent of “the Kennedy assassination or the King assassination.”

“He’s the biggest star in the N.B.A.,” Mr. George said. “He’s one of the biggest stars in professional sports, and he comes up with this disease, which at that time is an immediate killer. So even though he’s walking there and standing in front of everyone giving this press conference, as Karl Malone says, they think they’re seeing a dead man walking.”

Mr. George, who was then a New York Knicks season-ticket holder, said he recalled attending the team’s game that night against the Orlando Magic, where Pat Riley, then the Knicks head coach and the former coach of the Lakers, made a statement about Mr. Johnson and asked both teams to say a prayer for him. But, Mr. George said: “I don’t even remember anything else about that night. It wasn’t until we started working on the film that I realized the Knicks won the game.”

Two years later Mr. George learned that his sister, Andrea Williams, had been given a diagnosis of H.I.V. Ms. Williams, who is now an AIDS activist in Brooklyn and was the inspiration for Mr. George’s HBO movie “Life Support,” appears in “The Announcement,” as does Michael Weinstein, the president of AIDS Healthcare Foundation. Johnson friends and confidants like Arsenio Hall are also interviewed in the documentary, as are longtime fans like Chris Rock.

But getting Mr. Johnson to agree to his interviews, some of which were conducted at the Forum in Los Angeles, where he played as a Laker and disclosed his diagnosis, “was the key to everything,” Mr. George said.

“Between the time he was diagnosed and the time he announced was 10 days,” Mr. George said. “And in that 10 days there was so much drama involved within, whether to reveal, how do we reveal? We need to get a second opinion. What’s that going to be like? Is Cookie infected, will my pregnant wife be infected? Will my newborn child be affected? Before he got at that podium, there’s a whole world of drama that we were able to really depict in incredible detail.”

Why Haven't Condoms Evolved?

2012-02-12T12:12:00.000-08:00

andrewsullivan.thedailybeast.com
The pleasure-deadening devices "have not been significantly improved since the 1800s, when rubber first replaced the then-standard animal intestines." Paul R. Abramson and L.J. Williamson can't understand why:

[A]lthough we've been chasing an HIV-prevention vaccine since 1984, we've still got nothing to show for it. Imagine how far those same hundreds of millions could go toward the development of a better-feeling condom — a condom people would actually wear. After all, there is one area in which condoms don't suck: They prevent sexually transmitted infections. To date, we haven't even found a vaccine to prevent one of the many strains of HIV. Even if an omnipotent AIDS vaccine were developed, it would still leave untouched syphilis, gonorrhea, chlamydia and every other sexually transmitted infection. Compare that to the simplicity of the one-size-fits-all-diseases barrier method: the simple condom. Chasing a vaccine has so far been a losing game. But a great-feeling condom could be an epic win.

(Image: 110-year-old condoms made from the swim bladders of fish)

“Why have I to believe that the AIDS test meaning is equivalent to an infection with the HIV virus?

2012-02-12T09:01:00.000-08:00

ANALYSIS OF THE ANTIBODY TESTS
by: Fabio Franchi   Specialista in Igiene,   Medicina Preventiva   e in Malattie Infettive  Trieste
http://www.cesil.com/0898/enfrah08.htm

The tests of the antibodies we shall examine are the Elisa, the Western Blot, the p24 antigen capture assay.

ELISA (Pict. 1)

In Italy, the screening test (ELISA), “provided with a good sensibility (near 99%) and a lower specificity, valued about 90-95% in 1988”(4), is used at first to identify the HIV infection. However these percentages must not deceive, in fact the test predictive value changes depending on the infection prevalence in a certain population. According to a theory expressed in 1988 by the AIDS National Commission (4), in case of screening of the Italian prison population, in comparison with 6,902 real positive individuals there should have been 1.751 false positive; on the contrary, in case of blood donors, in comparison with 198 real positive, a good 999,990 should have been false positive (505 times more!). In the over mentioned text (2) the authors assert that the progressive improvements took sensibility of the test to 95% and its specificity to 99.8%, in high-risk population. Nevertheless they admit that “the positive predictive value can greatly fluctuate depending on the population they study”. Actually this happened. Depending on the information published on the English authoritative medical magazine The Lancet (5), in 1990 on 20.2 million ELISA tests made in Russia, 20,000 were positive, but only 112 were confirmed by the WB; in 1991, on 30 million ELISA tests, a good 30,000 were positive, but of these only 66 were confirmed by the Western Blot, that is a minimum percentage (0.002%).
“Then as the ELISA test has been planned to optimize the sensibility to the detriment of the specificity, it should not be used by itself for the HIV-1 infection diagnosis without a confirmation test (2), although in some Countries is used alone.

Western Blot (pict. 2)
The Western Blot is commonly used as a confirmation test of HIV infection; the combination of the Elisa and the WB should have a “positive predictive value higher than 99% for low-risk and high-risk population” (2).
However even the WB does not seem to be so specific as sustained if we analyze some data at our disposal.
A) Even official sources acknowledge that “for reasonable disagreements it was very difficult to code the definition on what a positive Western Blot should be considered” (2) . Since 1993, in United States there were just 5 official criteria, and only one (indicated in Du Pont's diagnostic kit) was approved by FDA (Food and Drug Administration). This was the most restrictive one and was used by a few laboratories. If only this criterion had been used , in United States only the 50% seropositive individuals would have been confirmed as really infected (6)! In Italy in a publication of the Health Ministry directed towards G.P. (7), the authors denied there had ever been such a problem. On this subject they affirmed: “in most cases, quite apart from the criterion used, the test results correctly coded when the individual is infect”.
The remedy to such a situation was found simply standardizing the different criteria without reconsidering the past and without explaining the scientific reasons for which they opted in that way.
Afterwards the CDC identified their criteria with the ASTPHLD's ones and in 1993 the United States Red Cross conformed adopting the ASTPHLD/CDC's advice”(2). “According to the American authority ASTPHLD, a positive result must present at least two of the three main bands of diagnostic meaning (antigp-41, anti-gp120/160, anti-p24)”.
B)The reading of the WB is visual and therefore is liable to interpretation from the operator, a variability factor not negligible. “Its technique (note: the Western Blot) was not standardized, the importance and the consequences occurred in the laboratories have not been yet measured.
Their results must be interpreted; the criteria for these interpretations vary not only from laboratory to laboratory, but even from month to month..” (8). The Consortium for Retroviral Serology Standardization (CRSS) made a quality control study*and sent 19 aliquots of the same serum to 19 different USA reference laboratories. Results comparison has shown an incredible differences of the number of bands and of their intensity (6) (pict. 3).
C) The antigenic preparations are not purified.
“The presence of bands in positions not corresponding to well-known virus antigens is a rather common finding and we suppose it is the consequence of contaminants in the preparation...” “The molecular weight of these aberrant bands may vary either from company to company or even from lot to lot of the same producing company” (2).
Here is Zolla-Pazner's comment in 1989: “A confusion on the identification of these bands (note: the results of the Western Blot test ) resulted in incorrect conclusions in experimental studies. [...] A re-interpretation of the already published results could be necessary”(9). Re-interpretation that has never been made.
D) The bands considered “specific” in many cases does not indicate an HIV infection. Some examples follow.
- Even if the more restricting criteria were employed, Lundberg noticed that 10% control sera, which included blood samples from blood banks, had a positive WB (6).
- A study(10) shows that from 2 to 49% tested patients can have a reaction to the WB (unspecified WB), more frequently caused by cross-reacting antibodies.
- A simple vaccination against flu can give a positive result too (11).
- Transfusion of own irradiated blood induces the formation of the same antibodies (12).
- Among the homosexuals and bisexuals who resulted negative for ELISA and PCR, 20%-30% can have either one or more bands present in the Western Blot.(2)
- There are even more amazing data concerning dogs and published in 1990. Writing on Cancer Research, Strandstrom at al. reported that 72/144 (50%) dog blood samples obtained by the Veterinary Hospital of the University, California, and tested with the Western Blot reacted with one or more HIV recombinant proteins [gp120--21.5%, gp41--23%, p31--22%.p24--43%]”(13). As the Authors think that dogs can not be infected with HIV, one must conclude that these data are a further prove of the frequent antibody cross-reaction with many proteins different from HIV ones”.
Remarks: The fact that the bands are considered unspecific if they are found separately, but virus-specific if they are present in a number of two or more, seems to refer not to considerations of a biological kind, but to a convention, a legal agreement changeable in time and space (in fact it is different from nation to nation). According to a convention accepted since a few time ago by many authors, three bands in a clinically healthy blood donor's WB were considered false positive reactions. According to the same convention, three bands of the same blood donor, this time presented to an Insurance Company for a life policy, should be considered true positive.
The researchers group from Perth who analyzed in depth the WB meaning, concluded that the proteins considered viral proteins are not peculiar to HIV, but one cannot distinguish them form proteins of a cellular source. In particular, according to the review by Eleopulos et al.(14) which has not yet been refuted up to now, the gp41 should correspond with actine; the p18 and p24/25 with the two myosin sub-units (p24 is the unspecific band found more frequently in “uninfected” individuals); the p32 should be identical to the beta chain of the antigen DR of the histocompatibility class II; the gp120-160 should not be other than gp41 oligomers.
The p24 antigen
In U.S.A. the evaluation of the p24 antigen capture test was included among the assays which are carried out to each blood unit (and it is considered as an “HIV direct evidence”). Fauci et al.(2) think that: a) the p24 corresponds to virus capsid antigen (core) which is highlighted by a serum containing the related monoclonal antibodies (anti-p24) associated to a detector system; b) however the test is not useful like a primary screening mean in establishing a precocious HIV infection diagnosis; c) the p24 level increasing corresponds presumably to the blast in virus replication, which can be observed by other methods like plasma viraemia; d) the p24 level usually falls under the determination threshold with conventional methods and like the antibody anti-p24 starts developing during seroconvertion and can remain in that state during the following asymptomatic infection years. Only 20-30% of the individuals with asymptomatic infection has detectable levels of p24 serum.
However there are many perplexities on its real meaning. Quantity data indicate that 50 pg and sometimes more of core protein (p24) may be found in seropositive patients. If a retrovirus weight is of 10-3 pg and half of its weight is constituted by p24 (15), then this quantity corresponds to about 100,000 viral particles, according to other authors and on other premises even to 500,000 particles (16)! Then if all this protein came from virions, these patients should be highly viraemic (17, 18). In other words there should be a direct correspondence among the p24 levels, “virus isolation”, “viral RNA” levels (said also “viral load”). On the contrary it is not so. Results are irremediably different from the ones one should expect. For example a paper reports the presence of antigenaemia, but that no virus could be isolated by 31 antigenaemic patients, even after an extended culture (19).
Other studies report similar remarks. We shall mention some of them:
1) in half of the cases when a person had a positive test, afterwards he had a negative one without making any treatment which could alter the p24 levels... the test is clinically erroneous and should be interpreted with much caution”.(20)
2) the p24 antigen is found neither in all seropositive subjects nor in individuals with clear AIDS. In a study , the PCR (Polymerase Chain reaction) and p24 were used to detect HIV in patients in in various stages, from asynptomatical to AIDS individuals. They found the p24 in 24% and HIV-RNA in 50% of patients (21).
3) More than 29% of the patients who receive a transfusion from seronegative individuals, become positive for the anti-p24 antibody (22), even “on infection absence”.
4) The unspecificity of the p24 antigen assay is so obvious to be accepted by an authority recognized in the field, Philip Mortimer.et al- from Public Health Laboratory Service in England.” “Experience proved that neither virus culture, nor p24 tests are of great value in diagnostic tests. They can be either insensible or unspecific” (23).
Conclusion
The antibody tests (the ELISA, Western Blot and p24 antigen capture assay) for the many reasons over explained, are non able to indicate with reasonable assurance they can face an HIV infection and so the assertion that WB positive predictive value (24) can be considered higher than 99% does not correspond with reality. These tests show reactions of a variable or rather undetermined specificity, so that they cannot allow a distinction between cross-reaction and “HIV infection”.
THE DIRECT IDENTIFICATION
OF THE VIRUS
It is a common conviction that the antibody tests should be ratified and in a certain way verified from other ones which are able to highlight the virus itself, tests able to identify it directly. However, this direct determination is such only apparently. It can only record some phenomena which are considered associated to the HIV in an unequivocal way. Virus direct identification is divided into 2 main categories (2): the virus culture and the direct identification of the viral nucleic acids (Southern Blot, amplification techniques like the PCR,TR PCR, bDNA, NASBA).
The viral culture
Usually virus isolation involves a patient's cell co-culture with a donor's uninfected cells which have been stimulated with phitoemoglutinine (PHA) for 3 days. These co-cultures are controlled about every 3 days for 28 days or more to control either the syncitia formation and p24 presence or the reverse transcriptase (RT) in culture supernatant (2). The presence either of syncitia (a) or the p24 antigen (b) or the RT (c) is considered a virus replication evidence (2). According to Gallo et other authors even the finding of virus-like particles in culture must be considered a sufficient criterion.
a) The appearance of sincytia.
Sincytia appearance is observed only in considered infected cultures, but these are present even in “uninfected” cell lines and are similar to the ones used for HIV (25). Then such morphological feature could be a characteristic either of the same cell lines, or of the result of the culture conditions or both these factors (14).
b) The p24 antigen.
Its specificity lack has already been mentioned. The objections to use it like a test on the patient's serum are efficacious even for its use in cultures. In a study where this “virus isolation” method was employed ( the determination of the p24 in cultures with unfractioned entire blood), positive results were obtained in 49 of 60 “presumably uninfected but serologically undetermined individuals”(82%) and in 5 of 5 seronegative blood donors (26).
c) The reverse transcriptase (RT).
In all the HIV research, the ability of copying template-primer A(n)dT15 - when it is incubated with the supernatant or material coming from infected material co-cultures with the AIDS virus which separates at a 1.16 gm/ml level (sucrose density gradient) - is considered the proof of a reverse-transcriptase activity of HIV. In many cases this activity is considered synonymous of “HIV isolation” . However: also the template-primer itself is copied when it is incubated with material which separates in 1.16 band from leukemic cell cultures (27) and uninfected spermatozoa(29); b) the template-primer A(n)dT15 can be transcripted not only by RT, but also by other DNA cell polymerases. All the DNA cell polymerases, alfa, beta and gamma are able of copying the A(n)dT15 (29). In fact. in 1975, an International Conference on DNA which included Baltimore and Gallo (30) on eukariotic polymerases defined the DNA polymerase gamma, “a normal cell component” (31) which activity can be increased by many factors including the PHA stimulation (32), an enzyme which “copies the A(n)dT15 with high performance, but does not copy well the DNA” (33). From what over explained we may deduce that it is wrong to affirm that such an enzyme activity is peculiar of retroviruses, and less that this is an unequivocal index of the presence of HIV. Particles and proteins which separate at 1.16 mg/ml band level could reflect fully unviral material, most of the same material is certainly cellular and coming from cultures stimulated with PHA (as we shall see better later), since transcriptase activity could derive from it.
d) Objects with a retrovirus appearance.
Gallo considered the finding of retrovirus-like particles in culture like the proof of the HIV isolation (at that time HTLV-III) (34). However Gallo used H9 (HUT78) cell line to isolate HTLV-IIIB, and this cell line releases retrovirus-like particles even when it is not infected with HIV” (35). Weiss obtained his “isolate CBL-1 from the leukaemic cell line CEM, a cell line which hosted retroviruses even when they were not infected with “HIV”(36). In 1970, these particles were frequently observed in leukaemic tissues (37), in embryonic tissue cultures (38, 39) and in most if not in all human placenta (40). Mature and *extrobended* particles of the C pattern appear in linphoma cells which are metabolically damaged but are not infected with HIV (41). “Retrovirus particles” antigenically similar to HIV were found in extracts from Sjorgen syndrome patient's salivary glands(42). And more important thing, in the only study of electron microscopy(43), both in vivo and in vitro where suitable controls were used and where an extensive assay in cieco of controls and test material was made, “virus particles indistinguishable from HIV were found” in a variety of reactive linphoadenopathies which are not HIV-associated, so that the authors concluded: “The presence of such particles does not indicate, for itself, an HIV infection”(pict 4).
Conclusion: it is inevitable to agree that neither syncitia presence, nor p24 finding, nor reverse transcriptase activity, nor virus-like particle presence (well, each element which settles that an HIV culture is positive) are “a virus replication evidence, though just this is the significance given to it.
Direct identification of the nucleic acids
For direct identification of the nucleic acids one intends the Southern Blot, PCR techniques, the quantitative amplification techniques (RT PCR, bDNA, NASBA). The identification is based on the identification and amplification of little nucleotide sequences attributed to HIV, not of the entire viral genome. This research is made not on cultures, but direclty on patient's tissues (including blood).
a) Southern blot technique (technique which allows to separate and highlight nucleic acids of the searched kind).
In 1984 Gallo carried out the first study. Using the Southern blot hybridization technique (capable theoretically of identifying only one infected on ten cells), AIDS patient's tissues were examined, but weak bands were found only in a minority of them (44).
b) The PCR (polymerase chain reaction).
The PCR sensibility is valued 92-100% (45) and is able to detect one “infected” cell on 100.000 (2). However, “for its high sensibility, it is greatly liable to false positivity either for even minimum contaminations or other common laboratory mistakes” (2). Retrovirus-like sequences can be found in human genome in every cell (46). Already in 1991, Imagawa and Detels pointed out a potential fallacy of the PCR. “The determination of a part of the genome- they affirmed- does not mean to detect an entire virus” (47).
The problem of the false positives.
Many researchers challenge the PCR reability for the great number of false positive that this test should produce(48). The PCR did not prove reproducible and false positives and false negatives were observed in all the 7 reference laboratories involved in an important French study (the concordance with serology varied from 40% to 100%). Moreover, the number of positive results was not significally different among high and low risk seronegatives (49). There are many other confirmations to these remarks:
1) A validity study in evaluating the HIV PCR performance and in identifying free-cell viral DNA showed “a disturbing high rate of unspecific positivity“ employing commonly used primers (SK38, both for the p24 and the gag gene). Really, similar positivity rates were found either for antibody negative samples than for antibody negative samples(18% against 26%) (50).
2) the PCR (qualitative DNA-PCR) made on uninfected infants appeared positive on many occasions (51).
3) In a PCR validity study coordinated by the OMS Work Group on the PCR, 54% of involved laboratories had problems with false positive results; 9.3% of uninfected samples were reported as positive(52).
4) The authors of a multicenter study of quality evaluation stated “this study showed that false positive results, in spite of rigorous procedure algorithms, happen among uninfected individuals with such a frequency to remain a serious problem”(53). The discover of a considerable number of “false positives” gives evidence of a remarkable PCR specificity lack.
c) Quantitative techniques.
The “quantitative” techniques” should be able to calculate, in an approximate way, the number of virions per milliliter of plasma using opportune modifications of some amplification techniques (either substrate amplification, like RT-PCR and NASBA, or signal amplification, like bDNA.The substrate consists in “preserved regions” of a virus-presumed gene. The calculated sensibility is: for the RNA RT-PCR of 100 HIV RNA copies per milliliter of plasma(2); for NASBA of 1,000 molecules per milliliter (54); for bDNA (branched DNA) of 10,000 molecules per milliliter (2). Up to 1994 HIV was considered to be present in small quantities in asymptomatic and AIDS subject's tissues (1 lymphocyte on 1,000-100,000). In 1995 two studies (55, 56) seemed, on the contrary, to show that HIV replicated with much activity since from the first phases of the infection. The over-mentioned techniques in appearance allowed huge virus quantities, which in a first time had escaped from observation, to be detected.
However if a massive infection were present in infected individuals, as some of the most known experts claim, the Southern blot hybridization would have been more than sufficient to detect it. Don't forget that “either virus DNA scarcity or lack in a considerable patient's part was a surprising result”(57). A John Maddox' significant Freudian slip confirms suspects: according to Maddox “both Ho than Wei and their colleagues were able to come to their alarming conclusions only after a ten years research of the HIV as they teamed up with mathematicians and because they were able to use new techniques to detect the low levels of virus involved “(58)!
Logical incompatibilities of results are macroscopic and evident.
A) In fact there is a lack of correlation between p24 and gene amplification techiniques. (We have already mentioned the fact that the p24 is considered to be “ the direct proof of HIV identification”).
A) No relation was found between the p24 level and the RT-PCR (59). The determination of the viral charge was highly sensible when it was compared with the p24 measurement (more than 95% of patients had detectable virus charge while only 40% had detectable p24), but in positive samples antigen and viral charge level had only a borderline significance (60).
B) No relation was observed between viral charge quantified either with the NASBA or the Amplicor and the concentration with the p24 antigen. No relation was observed between the infectious dose, the viral virl load found either with the NASBA or the Amplicor(RT-PCR) (61).
C)There is a relation lack between RT-PCR and other assays. In a study on vaccinated subjects, a group of four serum samples resulted positive with RT PCR during a 11 months period, including a result of 104-105 copies/mL, and an year later a fifth positive result in a vaccinated subject, but not infected” (62). For this reason, the authors advanced “doubts concerning specificity of HIV RNA measurement as a golden standard for the screening and the infection confirmation”.
D) There is finally a lack of correlation between “virus” and “viral load”.
1) According to Piatak, the high “virus” level in plasma was 999 per 1,000 “unculturable” (63).
2) Ho et al. showed that 10,000 plasma “virions” counted with the branched PCR correspond with less than one “infectious” virus per ml (64). 3
) In a more recent study by Ho (65) one may notice that 0 (zero!) “cultured viruses” corresponded to a load of 500,000 units! According to the reported data, to patient 105 before the treatment (with Ritonavir) 643,000 “virions”/ml were detected, where the number was calculated with the branched DNA assay, more than 1,000 TCID-50/ml corresponded to it (50% tissue culture infectious doses). After a two day therapy and in following days the “cultivable virus” was 0(zero). In the meantime, at 2, 3 and 4 days “free virions” (that is the so-called “viral charge”) remained over 500,000. Till 7 day “virions” were again over 100,000. A virion is defined as a complete viral particle constituted with the viral nucleic acid, capsid and pericapsid (when present). The possible objection for which a defective virion is “seen” by branched DNA assay, but is not detected by culture samples, does not resolve the problem of non-correspondence with the other tests and the impossibility of seeing these particles at the microscope directly from patient's tissues, without culture transfers. If it were so, Gallo would not need for applying to frauds (67, 68), he would not call for three year tireless researches in order to find something which had the appearance of a virus. He would have come to it immediately with other researchers.
Mark Craddock, professor at the School of Mathematics and Statistics, The University of Sidney, Australia commented: “What is this viraemia of billions of RNA particles that can only be seen with an undocumented branch-PCR or PCR but not with a functional infectivity test?”. (68)
VIRAL GENOME

As already stated, genomic amplification techniques concern small segments, not surely the complete “viral” genome and the results which are obtained do not give the assurance to have the true “HIV”, besides they are frankly discordant. At this point it's legitimate to ask what is really and how it's made the original viral genome. The reserch group from Perth (69) notes that if an unique AIDS retrovirus existed, then less than 1% genomic differences should be the rule, not the exception. For instance, the type 3 Sabin poliovirus vaccine differed from its neurovirulent progenitor at only 10 nucleotide positions after 53 in vitro and 21 in vivo passages in monkey tissues. In 1977, H1N1 influenza A virus reappeared in the human population after 27 years of dormancy with sequences mainly identical to those of the 1950s virus”. Although Eigen's quasispecies model has been used to describe the genome of RNA viruses, even 1% sequence differences in these genomes are considered to represent “extreme variability”. “Many selective forces may stabilize virus populations. These stabilizing factors may include the need for conservation of protein structure and function, RNA secondary structure, glycosylation sites, and phosphorylation sites”. Let us see what is the picture offered by HIV research. Not long afterwards it was discovered that “If you were to test two HIVpositive people at random and analyse the genetic material of their strains, they would differ, on average, by about 13 percent” (70). Besides what is considered to be the genotype of HIV comes from sequence analysis of subgenomes that   HIV genotype consignments are derived from sequence analysis of subgenomes measuring 2% to 30% of the total (71). The data is that such “genomes” vary between 3-40% (72,73). “If 30% of the HIV genome varies as much as 40%, how much does 100% of the HIV genome vary? This is the legitimate question of Eleopulos and colleagues (69).
Among researchers there is disagreement also about the number of HIV genes. In 1988 they said HIV genome had eight genes (74), in 1990 ten (75). In 1996 Montagnier referred that HIV had eight genes (76), and according to Barré-Sinoussi, HIV has nine genes (77) Not even the number of nucleotides of HIV genome seems to be constant (69)
HIV quasi-species
Because great genomic differences were found - even the same person can harbor more than 106-108 genetically distinct variants (78) - to try to find a justification for this phenomenon, the concept of quasi-species has been introduced. Prior to the 1990s, the HIV sequences were classified as African and USA/European with sequence differences of 20-30 percent between these two groups. (79). In the 1990s, HIV researchers started to divide the “HIV genome” into subtypes A, B, C, D, E, etc. The basis for this classification system is: “(a) subtypes are approximately equidistant from one another in env; (b) the env phylogenetic tree is for the most part congruent with gag phylogenetic trees; (c) two or more samples are required to define a sequence subtype”. However, “Subtype naming problems have arisen. A small but not insignificant number of viral sequences are hybrid, clustering with one sequence subtype in gag and another sequence subtype in env, for example;... Naming becomes problematic when highly divergent forms of a given subtype arises: such forms are sometimes designated A', B', F', etc”. It is increasingly necessary to have sequence data from both gag and env coding sequences when a new form or subtype is being claimed” (80). By the middle of 1996 “at least ten” (A-J) prevalent major (M) and a low prevalence, O, HIV-1 genotypes were described and new genotypes are still reported (81,82).
Is it possible then to describe the “HIV DNA” even if it has variation of 10% , not to mention 20 or 30 or 40% as is the case, as a ...”population of closely related genomes, referred to as a quasispecies” (69)? The extreme variability of HIV genome make us ask what is the sense to refer to HIV as a clear distinct entity. The genomic difference among human being of different race is about 1 per 1.000, between man and orang-utan about 2%, but to find a 30% difference is necessary to compare non the less man and mouse, man and ass, man and elephant! Can one consider mouse, ass and elephant as quasi-species of man? (pict. 5).
Particle detection Retrovirus are defined as particles of about 100-120nM of diameter with a core which includes a proteic coat and a ribonucleoprotein complex. Retroviruses are classified in three subfamilies: Spumavirinae, Lentivirinae and Oncovirinae. Retroviruses belonging to the last subfamily are divided in type A, B, C, and D particles. To which of these should belong HIV, is not very clear. According Gallo in 1984, it was a type C particle, but in 1985 he admitted it could be also a type D (83). Montagnier and coll. initially reported it was a type C particle (84), then a type D (85), and then a lentivirus (86), that is to say a different subfamily. According to Munn and others AIDS virus shows characteristics of type C, of type D and of lentivirus (87). Fauci and others described HIV in monocyte/macrophages cultures as retroviral particles with characteristics of type A (88). HIV identity seems to be so vague, so “shot”, that it adds further reasons of perplexity. Photographs Several researchers in the AIDS field have shown HIV photographs, but those that can be seen are only virus-like viral particles indistinguishable from normal cellular microvescicles. These particles, in contrast with viruses, are very unstable when removed from their contest, and it's difficult to isolate them and photograph them in a condition of a true isolation. On the contrary, viruses are stable because they have to leave again the cells and host organisms. The use of centrifugation techniques doesn't constitute a problem to separate viruses from various contaminants and so get their isolation - then photograph them, to put in evidence their proteins and their genetic constituents in a direct way. True viruses are so stable that it's easy to photograph directly them as tridimensional particles by an electronic scanning microscope, without the need to first fix them chemically. On the contrary, the microvescicles are so unstable that can be photographed only by a transmission electronic microscope which requires that they be previously fixed chemically in ultra-thin sections. What has been shown to the world as HIV micro graphs are ultra thin sections which include particles indistinguishable from the cellular ones (89) (pict 6-8).
The evidence of HIV (non-)existence A noteworthy confirmation to the argued critics of the researchers from Perth came in march 1997: two groups, one French/German (90) and one from the American NCI (91), have published the photographs of density gradients in which pure HIV virus had to be present (pict. 9). These data should have been available by the first isolation of the virus (1983-84), but nobody showed them before. The most likely reason is the lack of correspondence between what they found and what they expected.
In the Franco/German study the pictures are from the 1.16 gm/ml band. It is impossible to tell from which density the pictures in the American study are taken but presumably it's the same 1.16 density for retroviral particles. Eleopulos and colleagues note that “. The authors of both papers concede that the particles which are present in the banded material and which are said to be HIV represent only a very small fraction of the total material. Gelderblom et al. state that the material contains “an excess of [cellular] vesicles with a size range 50-500nm, as opposed to a minor population of virus particles... cellular vesicles appear... to be a major contaminant of HIV preparations enriched by sucrose gradient centrifugation”. “For the small number of particles deemed to be “HIV” no evidence is given that they are even a retrovirus-like particle. Indeed, to the contrary: (a) the particles do not appear to have surface spikes (knobs)... In other papers published by many researchers including Gelderblom and his associates such projections are noted to be absent (93, 94); (b) the particles referred to as “HIV” are not spherical and have diameters exceeding 100-120 nM. In the EM in Gluschankof et al. (90) there are arrows pointing to five “HIV” particles devoid of surface projections whose dimensions are 121 X 145; 121 X 169; 121 X 145, 121 X 145 and 133 X 145 nM respectively.
In Bess et al. (91) there are a total of six “HIV particles” also devoid of surface projections whose dimensions are 160 X 240; 200 X 240; 280 X 280; 208 X 250; 167 X 250 and 250 X 292 and nM respectively. “Actually, the authors maintain these are HIV particles, but without any proof. In the material of that density band there ought to be many viral particles, on the contrary they point only some, among many impurities.
They bear only the vaguest resemblance to retroviral particles”. “The point is that any genuine retroviral particle contains a fixed amount of RNA and protein. No more and no less. This means that if we consider diameters of particles pointed in the two studies, they are 1.14 times to 1.96 times larger than the estimated maximum for a normal HIV particle. Translating this in volumes, and comparing them to a particle with a diameter of 120nM, the Franco/German particles have 50% more volume than a retroviral particle and the US particles have 750% more volume”, that is to say incompatible with the same definition of a retrovirus! Even if the authors do not admit it, the data of the two cited papers contribute to show that where should be present pure HIV, of HIV there is no trace.
CONCLUSION
None of the tests examined seems to be sufficiently sure to detect an HIV infection. Paradoxically not even the “direct virus detection” is able to do answer to the same question. As a matter of facts there is an incompatible discordance among the results obtained with different methods. These discordances are by themselves logical incompatibilities that invalidate them. Besides, the existence of an entity that one can reasonably name “HIV virus” is not proved, as far as its proteins, its genome, its physical particle are concerned. The true meaning of the tests is better understood if its origin is examined. To show the existence of a new virus, both Montagnier group in 1983 and the group of Gallo in 1984 separated supernatant of cultures they considered infected in density gradients. They erroneously considered that the material that banded at 1,16 mg/ml was constituted by “pure HIV particles”. The proteins which were present in this band and were reactive with AIDS patients sera (but not only with their sera) were considered HIV proteins. In the same manner, a particular fraction of RNA which they found in the same band was considered the genome of the new virus. By then, some of these proteins are used to get the reagent for some kind of tests or as immunogens to produce in laboratory animals the antibodies used for other kind of tests ( similar procedure was followed to obtain RNA segments).
At this point the explanation of Gallo experiments in 1984 appears clearer: he used a mixture of proteins (believed to be viral but in fact cellular) to immunize the rabbits and obtain a serum which obviously reacted with the same proteins that were in the culture from which the initial mixture came (95).
In other words Gallo believed to show an hypothesis (the existence of the virus) with other hypothesis shown to be false (that is to say that inverse transcription activity, the presence of virus-like particles, the antibodies obtained in the way just mentioned were all virus specific).
In this way were born the tests which to-day are still used and perfectioned to put so engaging a diagnosis. An important prove of the correctness of this interpretation of the facts stays in the results that they obtained on mice and monkeys in 1991 (96).
In those studies, with the scope to evaluate a candidate vaccine, some laboratory animals were injected with cellular components from cultures which were “not infected by HIV”: the results were similar to those obtained with “the real vaccine” (i.e. with virus from “infected cultures”).
No significant difference was found, so that the comment - perfectly suited and still up to date of John Maddox - was: “AIDS research turned upside down”.
That is to say that it wasn't necessary at all to hypothesize the presence of a virus to obtain those phenomena.
Fabio Franchi
Specialista in Igiene,
Medicina Preventiva
e in Malattie Infettive
Trieste

Tenofovir, Leading HIV Medication, Linked with Risk of Kidney Damage

2012-02-12T08:45:00.000-08:00

By Steve Tokar www.ucsf.edu/news

Tenofovir, one of the most effective and commonly prescribed antiretroviral medications for HIV/AIDS, is associated with a significant risk of kidney damage and chronic kidney disease that increases over time, according to a study of more than 10,000 patients led by researchers at the San Francisco VA Medical Center and the University of California, San Francisco (UCSF).

Michael G. Shlipak, MD, MPH

The researchers call for increased screening for kidney damage in patients taking the drug, especially those with other risk factors for kidney disease.

In their analysis of comprehensive VA electronic health records, the study authors found that for each year of exposure to tenofovir, risk of protein in urine – a marker of kidney damage – rose 34 percent, risk of rapid decline in kidney function rose 11 percent and risk of developing chronic kidney disease (CKD) rose 33 percent. The risks remained after the researchers controlled for other kidney disease risk factors such as age, race, diabetes, hypertension, smoking and HIV-related factors.

For individual patients, the differences in risk between users and non-users of tenofovir for each year of use were 13 percent vs. 8 percent for protein in urine, 9 percent vs. 5 percent for rapidly declining kidney function and 2 percent vs. 1 percent for CKD. “However, these numbers are based on the average risks in our study population, and patients with more risk factors for kidney disease would be put at proportionately higher risk,” said principal investigator Michael G. Shlipak, MD, MPH, chief of general internal medicine at SFVAMC and professor of medicine and epidemiology and biostatistics at UCSF.

Patients were tracked for an average of 1.2 years after they stopped taking tenofovir. They remained at elevated risk for at least six months to one year compared with those who never took the drug, suggesting that the damage is not quickly reversible, said Shlipak. “We do not know the long-term prognosis for these patients who stop tenofovir after developing kidney disease,” he cautioned.

Q & A

Tenofovir, for Patients and Providers

The implications for patients already on or starting antiretroviral therapy are “mixed,” said Shlipak. “The best strategy right now is to work with your health care provider to continually monitor for kidney damage. Early detection is the best way to determine when the risks of tenofovir begin to outweigh the benefits.”

Shlipak noted that HIV, itself, increases the risk of kidney damage, while modern antiretroviral treatments clearly reduce that overall risk. “Patients need to be aware of their kidney disease risks before they start therapy, and this should influence the medications that they choose in consultation with their doctor,” he said. “For an otherwise healthy patient, the benefits of tenofovir are likely to exceed the risks, but for a patient with a combination of risk factors for kidney disease, tenofovir may not be the right medication.”

Tenofovir is used to decrease viral load and increase immune cell count in people infected with the virus. It is currently considered the preferred first line treatment for HIV because of its potency, overall low toxicity, and convenience of dosing. It is sold under a variety of names, by itself and in combination with other medications.

The study examined the medical records of 10,841 HIV-positive veterans in the national VA health care system who were new users of antiretroviral therapy from 1997 to 2007. It was published electronically in the journalAIDS on January 9.

Lead author Rebecca Scherzer, PhD, a researcher and statistician at SFVAMC and UCSF, said that the observational study was the largest and most conclusive indication so far of tenofovir’s association with kidney damage. “There have been a number of previous, smaller studies suggesting that this drug might be associated with kidney disease, but the results were mixed,” she said. “Those studies may have missed this association because they were too small, lacked appropriate lab data or excluded subjects with pre-existing renal impairment or risk factors for kidney disease.”

To be sure that tenofovir was the culprit, Scherzer and her colleagues looked for associations between 18 other antiretroviral medications and the same three measures of kidney disease: protein in urine, rapid decline in function and progression to CKD. None were associated with higher risk.

Shlipak noted that the study results are particularly strong because two of the risk factors – decline in function and CKD – indicate kidney function, while protein in urine indicates physical damage to the kidney. “These are independent markers,” he said. “To see the same drug cause both types of kidney disease gives you a very objective signal that something real is happening here.”

Shlipak emphasized that, despite tenofovir’s association with progressive kidney disease, it is an important component of effective antiretroviral therapy that may be required in many patients to control viral load.

The VA is the largest provider of HIV care in the United States, said Shlipak. “We could not have done this work without access to the VA’s system of electronic medical records,” he said. “In particular, the data kept by the VA Clinical Care Registry, located at the VA Palo Alto Health Care System, were essential to this study.”

Co-authors of the study are Michelle Estrella, MD, of Johns Hopkins School of Medicine; the late Andy I. Choi, MD, MAS, of SFVAMC and UCSF; Steven G. Deeks, MD, of San Francisco General Hospital; and Carl Grunfeld, MD, PhD, of SFVAMC and UCSF.

The study was supported by funds from the National Institutes of Health, the National Center for Research Resources, the American Heart Association and the Department of Veterans Affairs, some of which were administered by the Northern California Institute for Research and Education.

NCIRE - The Veterans Health Research Institute - is the largest research institute associated with a VA medical center. Its mission is to improve the health and well-being of veterans and the general public by supporting a world-class biomedical research program conducted by the UCSF faculty at SFVAMC.

SFVAMC has the largest medical research program in the national VA system, with more than 200 research scientists, all of whom are faculty members at UCSF.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

HIV Experts Propose New Pathway for Conducting Phase 3 Drug Trials

2012-02-08T17:52:00.000-08:00

By Forum for Collaborative HIV Research

WASHINGTON , Feb. 7, 2012 -- New Approach Intended to Remove Barriers to Innovation in Drug Development

WASHINGTON, Feb. 7, 2012 /PRNewswire-USNewswire/ -- As the war on HIV/AIDS begins its fourth decade, and NO CURE and NO one has lived with these current DRUGS, medical researchers, pharmaceutical manufacturers, patient advocates and government regulators face a new and unexpected scientific challenge: how to demonstrate the safety and efficacy of promising new antiretroviral drugs when the two traditional study designs – the superiority trial and the non-inferiority trial – are no longer useful in showing improvements in both "treatment experienced" patients and those who have never received drug therapy (treatment-naive patients).

Because this challenge could have a dampening effect on what is now a robust drug developmentpipeline for HIV, the Forum for Collaborative HIV Research has just released a new scientific paper that lays out a substantially different approach for conducting Phase 3 HIV clinical trials.

Published in the journal AIDS, the paper summarizes the insights of specialists from the Food and Drug Administration, European Medicines Agency, academia, the patient advocacy community and industry that overcoming the current difficulties in conducting new HIV drug trials requires moving from the large-scale study model to a new approach where clinical improvements are demonstrated through a sequence of short, step-wise efficacy and safety studies.

"Despite the many valuable antiretroviral drugs now available to treat HIV, new antiretrovirals can bring important benefits, such as fewer side effects, less frequent dosing and a lower risk of drug resistance. That is why overcoming the barriers to innovation in HIV drug development is so critical," said Veronica Miller, Ph.D., Director of the Forum and one of the authors of the paper. "Our paper offers a new pathway for regulatory approval of promising new HIV drugs and reflects the best thinking of the top experts in the field."

The new pathway described in the paper calls for a multi-phased study design, which includes:

A short study (10-14 days) comparing the investigational compound versus placebo, with the patient's current failing regimen as background, to evaluate short-term efficacy in viral load reduction
A follow-on study where all participants receive the investigational drug (at a single or different doses) and are assessed at 24 weeks to evaluate dose response, safety, durability of initial response and development of resistance
The possibility of a second comparative safety trial in patients with a minimum of two active drugs available where participants are randomized to the investigational agent plus a new optimized background regimen of antiretroviral drugs versus patients on a new optimized background regimen plus placebo

Intended to preserve innovation in HIV drug development, the new proposed pathway focuses specifically on trials in multi-drug resistant patients, where rates of accrual into HIV clinical trials have declined precipitously, due largely to the increasing use of boosted protease inhibitors and the overall enhanced potency and efficacy of antiretroviral regimens. From 2006 to the present, the rate of patient recruitment for trials of treatment-experienced participants with multiple drug resistance has fallen from 1.15 per month to 0.02 per month even though sponsors are using an ever increasing number of study sites and countries. For these patients, the new approach of a short, step-wise superiority trial allows sponsors to demonstrate efficacy before the risk of developing resistance to the new drug or additional resistance to the old drugs can take place.

These new options are not as promising for conducting studies in treatment-naive patients, where results of both superiority and non-inferiority trials are difficult to interpret. With superiority trials, the challenge is that current first-line antiretroviral regimens produce viral suppression rates exceeding 90 percent in this patient population, making these studies impractical. With non-inferiority trials, the problem is that true differences between drug regimens can be difficult to interpret. For these reasons, there is no consensus on the utility of studying investigational agents in this patient population, although scientists, regulators and drug sponsors recognize these HIV drugs may offer treatment-naive patients better tolerability or reduced long-term safety risks than currently available options.

Reflecting the realities of today's environment, the new paper notes the availability of a wide range of antiretroviral agents -- 26 unique antiretroviral drugs (plus alternative formulations and fixed-dose combinations) from six different therapeutic classes – which collectively have produced viral suppression rates of between 70 percent and 90 percent. But the paper also reflects the growing problem of drug resistant strains of HIV and the ongoing need for new treatment options. Accordingly, the proposed changes in HIV trial design are intended as a pathway for regulatory approval of promising new drugs that will address multi-drug resistant virus while also offering patients advantages in safety and tolerability for patients.

The new scientific paper, "Novel Clinical Trial Designs for the Development of New Antiretroviral Agents," appears in the February 1, 2012 electronic issue of the journal AIDS (doi: 10.1097/QAD.0b013e3283519371; accessed February 6, 2012).

About the Forum for Collaborative HIV ResearchNow part of the University of California(UC), Berkeley School of Public Health and based in Washington, DC, the Forum was founded in 1997 as the outgrowth of a White House initiative which called for an ongoing collaboration among stakeholders to address emerging issues in HIV/AIDS and set the research strategy. Representing government, industry, patient advocates, healthcare providers, foundations and academia, the Forum is a public/private partnership that is guided by an Executive Committee that sets the research agenda. The Forum organizes roundtables and issues reports on a range of global HIV/AIDS issues, including treatment-related toxicities, immune-based therapies, health services research, co-infections, prevention, and the transference of research results into care. Forum recommendations have changed how clinical trials are conducted, accelerated the delivery of new classes of drugs, heightened awareness of TB/HIV co-infection, and helped to spur national momentum toward universal testing for HIV. http://www.hivforum.org

SOURCE Forum for Collaborative HIV Research

HIV/AIDS Vaccine from Canada received the green light by U.S. FDA officials to begin Human Trials

2012-02-08T11:08:00.000-08:00

By DAVE SMITH The International Business Times
Canadian researchers from the University of Western Ontario in London claim they have developed a promising HIV vaccine, which has received the green light by U.S. FDA officials to begin testing on humans.

"We started the basic science research two decades ago,"said Dr. Chil-Yong Kang, the lead researcher for the project. "The vaccine development, we started 10 years ago. This is incredible for us to get to this stage of development."

This HIV vaccine, called "SAV001," was developed with the support from Sumagen Canada, a biotech company designed to drive clinical development of Kang's work. It is the only HIV vaccine currently being developed in Canada.

The first of three clinical trials began in January, which used 40 volunteers that already had the HIV virus. The experimental medicine was awarded funds on Jan. 12 to support clinical trials of the vaccine

Unlike other attempts to create a "cure," this experimental medicine uses the entire HIV virus to create a "non-pathogenic" version of the microbe, which doesn't cause HIV in recipients. Instead, the vaccine primes the body's T-cells to destroy any cells that become infected with HIV. This same strategy has been applied to other diseases like polio, rabies, hepatitis A and influenza.

"In the past, people did not use this strategy because people did not know how to make a safer virus and people did not know how to make large quantities of it," Kang said. "Now we have solved those problems by the genetic engineering of the virus."

The vaccine has been successful thus far: Lab animals demonstrated a strong immune response in preliminary toxicology tests, and the FDA received approval to begin testing on humans in December 2011.

After more funds were awarded in January, Sumagen Canada received an extra $728,000 from the National Research Council of Canada Industrial Research Assistance Program (NRC-IRAP) to move to Phase II. The money was granted under the Canadian HIV Technology Development (CHTD) Program and the Bill and Melinda Gates Foundation, which recently pledged $750 million to the global AIDS fund on Jan. 27.

"These are tough economic times, but that is no excuse for cutting aid to the world's poorest," said Microsoft chairmanBill Gates at the annual meeting of the World Economic Forum in Davos, Switzerland.

The second phase of trials will measure immune responses to the vaccine in HIV-negative patients. After that, Phase III would test the effectiveness of the vaccine in a large group of 6,000-plus humans who could be at risk for becoming infected with the virus. In that experimental group, half of the participants would be given the vaccine and the other half a placebo. The researchers hope to track those volunteers for three years to see how many in each group become infected with HIV.

"The important thing for us is to have the support of the government of Canada for what we are doing," said Doris Hall, a representative from Sumagen. "I think it is important for Canadians to understand there is government backing."

For instance, a large Thailand study revealed that an experimental vaccine only helped protect against infection in about one-third of recipients. Those researchers are still working to improve that vaccine.

Of course, Kang's team of researchers are not the only ones looking to develop a cure for one of the world's most dreaded diseases. Several pharmaceutical companies and academics have developed potential HIV vaccines, but all of them have resulted in failure.

In Africa, researchers tested a daily HIV prevention pill called Truvada in thousands of native women, but the study was halted after results showed the pill was ineffective.

According to the World Health Organization, 34 million people around the world live with HIV, and 2.7 million people are infected each year. Yet in America, black men and women make up 46 percent of all HIV cases in the country, despite only representing 14 percent of the total U.S. population. By the end of 2008,AIDS had killed more than 240,000 black Americans.

In 2009, the Centers for Disease Control and Prevention said 85 percent of black women, who are about 15 times more likely to have the disease compared to white women, acquired HIV through heterosexual intercourse. HIV is strongly associated with urban poverty areas in the nation's major cities, and since those areas have limited access to quality health care, housing, and HIV education, 46 percent of blacks and 40 percent of Hispanics that live in those areas are at a higher risk to contract the virus.

The International AIDS Vaccine Initiative said there are more than 30 HIV vaccines around the world currently being tested in phase I clinical trials. Dr. Patrick Dakum, the executive secretary of the Institute of Human Virology (IHVN) in Nigeria, said he believes a viable HIV vaccine will be ready in the next five years.

To report problems or to leave feedback about this article, e-mail: d.smith@ibtimes.com
To contact the editor, e-mail: editor@ibtimes.com

Those with HIV obliged to disclose status to sexual partners

2012-02-08T06:58:00.000-08:00

From Wednesday's Globe and Mail

At the heart of the HIV disclosure case before the Supreme Court of Canada on Wednesday is the notion that those infected have a right to privacy and autonomy – a right that manifests itself in not having to tell a prospective sex partner that they have HIV: If the infected individuals are receiving effective treatment or if they use a condom, it’s their right to remain, as it were, silent.

This is a misguided view of individual rights. Autonomy should not give people with incurable illnesses the right to put others at risk. Privacy should not mean that infected individuals may bypass consent, without which sex becomes sexual assault. Rights do not exist in a vacuum. Individuals have obligations, too, and those include the obligation not to physically hurt others, and not to willfully or recklessly spread disease.

HIV advocates say the disease no longer poses a “significant risk of serious bodily harm” – a key phrase in a 1998 Supreme Court case on HIV disclosure before sex. Treatment or condoms should be enough. The Manitoba Court of Appeal accepted this argument in a case now before the Supreme Court.

In that 1998 case, the current Chief Justice, Beverley McLachlin, called the failure to disclose HIV infection an act that “shocks the conscience.” Today, the risk of HIV transmission for unprotected sexual intercourse still ranges from 1 in 2,000 to as high as 1 in 384, and condom use, though reducing those numbers further, is also prone to failure. These numbers still mean a “significant risk,” as most informed people would define it. One in 384, over and over again, is a frightening risk with an incurable disease.

The onus belongs on those infected with HIV, not on their sexual partners. That is an onus that this country’s HIV advocates do not want to accept. If their view holds sway, many people would be left exposed to the possibility of life-altering disease, and the vulnerable would be especially at risk. In one of the cases before the Supreme Court, the accused gave alcohol and drugs to low-income aboriginal young women, teenagers and a 12-year-old girl, in exchange for sex. All except the 12-year-old later said they would not have had sex with him had they known his HIV status.

The right to give or withhold consent to sexual intercourse is the autonomy issue at stake.

HIV Tests Are Not HIV Tests. WHAT?

2012-02-07T10:25:00.000-08:00

HIV tests do not detect HIV or HIV antibodies. HIV tests detect antibodies. Period. Test manufacturers claim that their tests are 99 percent accurate for sensitivity and specificity.

SENSITIVITY measures how often a test is positive when you already know what you are testing for is present. SPECIFICITY expresses how often a test is positive when a patient DOES NOT have the condition.

In all HIV test literature, sensitivity and specificity are not based on measurements of the test against an isolated virus, but is a concordant measure between two tests that do not detect HIV or HIV antibodies. Careful examination of the manufacturer’s label information makes this clear contrary to their claims of sensitivity and specificity of 99.9 percent. The vast majority of these reported measures of accuracy have nothing to do with whether HIV is present, but how well one test performs as compared to other tests already on the market. These measures of accuracy refer to the concordance between two tests; namely, how often a new test says a sample is positive when one already on the market says it is positive (sensitivity), and how often it is negative (specificity). Given the fact that all HIV antibody tests are based on the same molecular principles and built from the same portfolio of basic molecular building blocks, their remarkable concordance is not surprising.

However, even if two different tests demonstrate 100 percent concordance, that does not justify the use of either for purposes other than what they have been validated and approved for. By analogy, if two different manufacturers were to construct two different timepieces using the same specifications for the gears and wheels, only to put them in different casings, it is very likely that these two clocks would perform quite similarly. However, even if there were greater than 99.9 percent concordance between these two timepieces, one cannot conclude that either clock measures time accurately.

HIV tests are so notoriously inaccurate that ALL FDA-approved HIV test package inserts warn clinicians that persons who test positive can only be “PRESUMED to be infected.”

“Clinically indicated” means that diagnosticians must rule out dozens of other conditions and factors that are known to cause false positive HIV test results. Some of those conditions include:

Normal human ribonucleoproteins (48, 13)
Pregnancy (58, 53, 13, 43, 36, 85, 92)
Pregnant Latina women (97)
Receptive anal sex (39, 64)
Maternal antibodies carried over to uninfected infants (87)
Naturally-occurring antibodies (5, 19)
Rheumatoid arthritis (14, 62, 53)
“Sticky” blood (in Africans) (38, 34, 40)
T-cell leukocyte antigen antibodies (48, 13)
Blood transfusions, multiple blood transfusions (63, 36, 13, 49, 43, 41)
Hemodialysis/renal failure (56, 16, 41, 10, 49)
Organ transplantation (1, 36)
Renal transplantation (35, 9, 48, 13, 56)
Flu and other vaccines (30, 11, 3, 20, 13, 43, 72, 76 28, 21, 40, 43 67 40, 107, 108, 109)
Diabetes (101)
Drug abuse — Injection drug use (parenteral substance abuse & OTHER (86)
Hemophilia (10, 49)
Multiple sclerosis (86) (105)
Primary biliary cirrhosis (43, 53, 13, 48, 104)
Renal (kidney) failure (48, 23, 13)
Rheumatoid arthritis (36)
Epstein-Barr virus (37, 90)
Flu (36)
Malaria (6, 12, 75, 88)
Other retroviruses (8, 55, 14, 48, 13)
Stevens-Johnson syndrome (9, 48, 13)
Syphilis (101)
Trypanosoma cruzi (Chagas Disease) (88)
Tuberculosis (25)
Upper respiratory tract infection [cold or flu] (11)

*republished from omsj.org

* Also read more by Henry H. Bauer, Ph.D. http://www.jpands.org/vol15no1/bauer.pdf

Ask for the Kit insert before your next HIV and AIDS test.

2012-02-05T09:12:00.000-08:00

Learn more : A Selection of HIV Documents

Karri Stokely. Long Term Survivor HIV, on why she won't be quiet. Part 2

2012-02-05T08:32:00.000-08:00

Part Two of Karri Stokely's gripping talk, delivered in Oakland, CA, Rethinking AIDS Conference, November 6-8, 2009

Karri's Story: http://www.livingwithouthivdrugs.com/karri.htm

or visit http://www.karristokely.com/

Karri Stokely speaks at Rethinking AIDS Conference, Part One

2012-02-05T08:25:00.000-08:00

Part One of Karri Stokely's gripping talk, delivered in Oakland, CA, Rethinking AIDS Conference, November 6-8, 2009

Karri's Story: http://www.livingwithouthivdrugs.com/karri.htm

or visit http://www.karristokely.com/

HIV and AIDS: The U.S. vs. Germany

2012-02-03T08:54:00.000-08:00

Hey Tom,

Did you ask why we keep ignoring the fact that NO ONE has been cured, yet as you discovery more and more people are dying from AIDS DRUGS...?

"Doctors say they're also seeing other AIDS-related illnesses, like lymphoma and heart disease, become bigger problems in patients they're treating."

WTOP's Thomas Warren recently traveled to Germany for a fellowship with the RIAS Berlin Kommission. While there, he conducted research on the history of HIV in Germany, including the governmental policies aimed at handling the disease and how the virus is treated medically. As we continue our series, he takes a look at the German system and how it compares to the U.S.

Thomas Warren, wtop.com

WASHINGTON - Washington, D.C. and New York City both are recognized as having an extremely high prevalence of HIV infections in the U.S. Out of their combined populations of just under 9 million people, 123,000 are living with the virus, according to health department statistics from both cities.

By comparison, that's 56,000 more than in the entire country of Germany, which has a population of nearly 82 million people.

The number of new infections that occur in the U.S. each year also is 56,000, according to the National Institute of Allergy and Infectious Diseases.

"It's a small disease in Germany, but we know it's a dormant tiger," says Dr. Rolf Rosenbrock, a member of Germany's national AIDS advisory board.

Though Berlin is Germany's capital city, more cases are found in other cities such as Cologne, Dusseldorf and Frankfurt. The first cases of HIV/AIDS in Germany popped up in the southeast section of Munich in 1982.

Much like in the U.S., there was a societal stigma attached to HIV in Germany.

Rosenbrock -- who helped develop Germany's HIV/AIDS health care system with new training and treatment platforms -- says early policy discussions included talk of setting up separation camps and even tattooing people who were infected, though that never happened.

To keep HIV from becoming an epidemic, experts in Germany credit the creation of advocacy organizations within the gay community.

"The so-called 'gay men's movement' was to a certain degree strengthened," says Dr. Elisabeth Pott, director of the German Federal Center for Health Education in the Federal Ministry of Health.

She says strong collaboration between the gay community and federal agencies was central to helping keep infection rates low, as the virus began to spread to other German cities in the mid- to late 1980s.

As D.C. Councilmember Jim Graham points out, that did not happen in the U.S.

"At the heart of it all was homophobia. 'Distaste' is too kind a word. It was a hatred of gay people," he says.

German medical officials say the structure of their almost universal health care system is also a tool that has helped a large number of HIV-positive people get treatment early.

"Around 95 percent of the population has some kind of health care," says Dr. Ulrich Marcus with the Robert Koch Institute, which also is part of Germany's Ministry of Health.

The District, for all of its struggles in combating the HIV epidemic, is on par with Germany when it comes to its residents having health coverage.

"Ninety-three percent of adults have health insurance," says Dr. Gregory Pappas, senior deputy director of the District's HIV/AIDS, Hepatitis, STD, and TB Administration.

Pappas also says the city is tops in the nation in health care for kids under 18.

Germany, meanwhile, had just over 3,000 new infections in 2009, according to the Ministry of Health. The country has been able to stabilize new infections at around 3,000 since 2007.

But a concern in the German medical field is that the attention devoted to HIV/AIDS over the last 20 years has allowed other sexually transmitted diseases to become potentially major issues. Something we don't talk enough about

"We have Hepatitis C, which is not much easier than the HIV thing," Rosenbrock says.

Doctors say they're also seeing other AIDS-related illnesses, like lymphoma and heart disease, become bigger problems in patients they're treating.

Europe is known for its liberal views towards sexuality, and Pott says a central theme in Germany's strategy to prevent the spread of HIV/AIDS is a straightforward approach when discussing the consequences of risky sexual behavior.

"We do not try to patronize people. We tell them there are risks. We give you the information, but it is in your responsibility," Pott says.

THE SCHONEBERGER MODEL

In Germany, there's a three-pronged approach to care for HIV-positive patients.

First, a newly diagnosed person is not typically treated in a hospital, unlike in in the U.S. Instead, they're treated by a private doctor in the patient's own home.

"The private office does the primary care. If something goes wrong, and the patient needs to go to the hospital, then the hospital doctors and team take it over," says Dr. Keikawus Arasteh, chief physician at the Vivantes Auguste-Viktoria-Klinikum Hospital in Berlin.

There is also not much contact between private doctors and hospitals.

"They have a contact, of course, but it's a very light contact, not comparable to the U.S.," Arasteh says.

The contact they do have includes reports and updates on a patient's condition.

The treatment model is not one-size-fits-all. Arasteh, who has worked in HIV/AIDS research in Berlin since 1984, says the lower the T-cell count, the more likely a patient will be admitted to a hospital. He credits the development of new treatment drugs with aiding the model's success.

Having nurses able to administer treatment in a patient's home, in the absence of a doctor, is another unconventional facet of the Schoneberger Model.

"This was, for Germany, a revolution that nurses do treatment without a doctor on their side," Arasteh says.

The second tier of the model deals with treatment measures. As anti-retroviral drugs to treat HIV have been developed over the years, along with medications to treat other sexually transmitted diseases, infected patients are given priority to receive those treatments.

The third part of the Schoneberger Model involves when patients are admitted to the hospital. At one time, patients needed to show three to four AIDS-related illnesses before they were taken to a hospital, Arasteh says.

However, when doctors noticed patients were coming in seemingly on death's door, that requirement was modified.

"Now, we have patients who have 1.3 AIDS-related illnesses when they're transferred to the hospital," Arasteh says.

The dynamic of the model was created from the tragic early days when HIV/AIDS first appeared in Germany.

"In the former times we don't have many medical things to offer, and often patients died in the hospital," Arasteh says. "And the patients didn't like it, and we didn't like it."

WTOP's Thomas Warren's week-long series "Generation Positive" is an in-depth look at the HIV epidemic in the U.S. and Washington, D.C. In a four-part web series and an eight-part series on-air, he will be taking a look at measures being taken to beat HIV/AIDS and breakthrough developments in the search for a vaccine.

At 12 p.m. Thursday, Feb. 2, Dr. Gregory Pappas of D.C.'s HIV/AIDS Administration will take your questions on HIV/AIDS in the District and how it's affecting your community.

We will hold the live chat on WTOP's website.

Follow WTOP on Twitter.

You can email Thomas at twarren@wtop.com

Gilead Sciences 4Q profit rises on HIV drug sales

2012-02-03T00:01:00.000-08:00

www.cbsnews.com
(AP) FOSTER CITY, Calif. — Gilead Sciences Inc.'s profit grew 6 percent in the fourth quarter on greater sales of its HIV drugs including Atripla.

Gilead said Thursday that its profit rose to $665.1 million, or 87 cents per share, from $629.4 million, or 76 cents per share, one year ago. Excluding acquisition, restructuring, and stock-based compensation expenses, Gilead said it earned 97 cents per share, far short of analyst estimates for $1.05.

Shares of Gilead fell 56 cents to $48.75 after hours after rising 16 cents to $49.31 during Thursday's regular trading session.

Revenue grew 10 percent, to $2.2 billion from $2 billion. Analyst expected $2.18 billion

The company said its antiviral drug sales rose 9 percent to $1.86 billion. Sales of Atripla grew 11 percent to $863.3 million. Sales of Viread held steady at $190.9 million, and sales of Complera, which was approved in August, totaled $19.7 million.

Sales of Gilead's heart drug Letairis grew 23 percent to $78.7 million, and sales of Ranexa for angina rose 23 percent to $83.7 million. Sales of other products held steady at $151.1 million.

On Jan. 17, Gilead bought hepatitis C drug developer Pharmasset for $11.1 billion. Pharmasset is studying several experimental treatments for hepatitis C, including PSI-7977, a pill that is seen as promising. Doctors may be able to prescribe the pill as part of a regimen that does not include interferon, an injection that is a staple of hepatitis C treatment that causes difficult side effects.

The hepatitis C virus can cause life-threatening liver damage and it is the main cause of liver transplants in the United States. Analysts expect it to become a bigger health problem as baby boomers age.

In 2011, Gilead Sciences said its profit slipped 3 percent, to $2.8 billion from $2.9 billion. Earnings per share grew to $3.55 from $3.32 as Gilead bought back around 83 million shares. Revenue rose 5 percent, to $8.39 billion from $7.95 billion.

Open Letter to FDA Urging PrEP Review of the drug Truvada from AFC and 25 other HIV-AIDS Industry organizations

2012-02-02T10:05:00.000-08:00

Is this AZT all over again?

Seem like AIDS Healthcare Foundation is supporting the ideology of this blog?

Please support their efforts:

Send your eletters TODAY. Go to: www.nomagicpills.org

This is an open letter to the Food and Drug Administration, urging the priority review of the drug Truvada for use in PrEP (pre-exposure prophylaxis). The AIDS Foundation of Chicago and 25 other organizations signed this letter to counter the AIDS Healthcare Foundation's protest of the FDA regarding this review. To read the PDF of the letter, with footnotes, click here.

January 25, 2012

Margaret A. Hamburg, M.D.
Commissioner
Food and Drug Administration
5630 Fishers Lane
Rockville, MD 20852

Re: Request for Priority Review – Supplemental NDA submission by Gilead Sciences, Inc.
requesting approval of a labeling change to include HIV prevention indication use for
emtricitabine; tenofovir disoproxil fumarate fixed dose combination

Dear Commissioner Hamburg:

We write as a coalition of 25 leading HIV/AIDS and health organizations to request that
FDA grant priority review of a supplemental New Drug Application1 (sNDA) for the
approval of emtricitabine/tenofovir disoproxil fumarate (Truvada®) fixed dose combination
for pre-exposure prophylaxis (PrEP) to reduce the risk of HIV infection among adults as part
of a comprehensive prevention package including risk reduction counseling and condoms.
The rigorous priority review process applicable to efficacy supplements is the best means to
promote public health by recognizing the potential of PrEP to offer a major advance in HIV
prevention and deserving this priority “where no adequate alternate therapy exists or as a
significant improvement compared to marketed products … including nondrug products or
therapies.”

Our organizations understand that granting priority review is not tantamount to a final
approval. Nevertheless, we are hopeful that the full dossier of data on
emtricitabine/tenofovir disoproxil fumarate fixed dose combination of PrEP from multiple
clinical trials in different populations can lead to a responsible regulatory and marketing plan
that allows safe use in the populations that may benefit from this innovative development.

The need for significantly improved safe and effective HIV prevention tools is clear. Despite
many years of efforts to reduce HIV incidence using available counseling methods, some
50,000 new infections occur annually. Disparities persist so that incidence continues to
concentrate among African Americans and Latinos, men who have sex with men (including
transgender individuals), and the poor. These grim and stubborn facts led to the creation of
the White House-directed National HIV/AIDS Strategy for the United States (NHAS), which
lists enhanced prevention efforts as a primary objective. If emtricitabine/tenofovir
disoproxil fumarate for PrEP satisfies FDA approval criteria, health programs and individuals
will have improved choices to address a domestic priority and save lives.

The PrEP sNDA for Truvada® meets criteria set out in FDA’s Manual of Policies and
Procedures for priority review. As organizations committed to ending the AIDS epidemic,
we appreciate how the history of FDA’s regulatory tools for fast track approval or for
accelerated and priority review4 introduced the current suite of HIV therapeutic drugs to treat
active infection. In the present case, there is a clear unmet need for new effective methods
for preventing HIV infection, a need that is as urgent today as was the need for HIV
therapeutics over the past two and more decades.

HIV advocacy organizations made it possible to launch such regulatory procedures for the
benefit of all patient disease groups when those tools were not yet available. We are not
aware of any legitimate reason to thwart the faster introduction of medicines FDA determines
to be safe and effective to stop HIV, nor should anyone turn back the pages of history and act
against the interests of patients to do so now. Unfortunately, recent actions by the AIDS
Healthcare Foundation regarding PrEP would introduce unwarranted roadblocks in the FDA
process of making responsible decisions about potentially useful medicines and public health.
Those actions also foster misunderstandings of the careful balancing of risk and benefits that
informs a mature marketing permission based on all available data. Those actions would also
set an unhelpful precedent as PrEP research evolves in the future and the FDA is asked to
review non-tenofovir-based regimens (e.g. maraviroc), microbicide gels, and intermittent
PrEP. We urge that FDA continue its public health promotion goals now in the service of the
critical need to prevent, as well as treat, HIV and grant this priority review.

We would be happy to discuss the priority review process as applied to HIV prevention
further at your convenience. Mitchell Warren, Executive Director of AVAC, acts as the
contact person for the organizations signing this letter and can be contacted at 1-212-796-
6423 and mitchell@avac.org.

Yours sincerely,

AIDS Foundation of Chicago

AIDS Legal Referral Panel

AIDS Resource Center Ohio

AIDS Research Consortium of Atlanta

AIDS United

amfAR, The Foundation for AIDS
Research

Asian & Pacific Islander Wellness Center

AVAC: Global Advocacy for HIV Prevention

Black AIDS Institute

Caracole, Inc.

Chicago Black Gay Men’s Caucus

Fenway Health

HIV Prevention Justice Alliance

International Rectal Microbicide Advocates

Justice Resource Institute

LA Gay and Lesbian Center

Multicultural AIDS Coalition

National Alliance of State and Territorial
AIDS Directors

National Black Gay Men's Advocacy
Coalition

National Latino AIDS Action Network

National Minority AIDS Council

Ohio AIDS Coalition

Project Inform

San Francisco AIDS Foundation

SisterLove, Inc.

Ursuline Sisters of Youngstown

HIV/AIDS Ministry

Us Helping Us

Saliva HIV Test As Effective As Blood Test: Study

2012-01-31T10:00:00.000-08:00

Here we good more PR to push Testing:

www.huffingtonpost.com

Despite advances in the treatment of HIV, one huge challenge still lingers in the medical community: getting people tested in the first place.

The stigma associated with being tested and potentially exposed in a public clinic has prompted scientists at the Research Institute of the McGill University Health Centre to evaluate the efficacy of an oral HIV self-test, a method they believe can serve as an effective but much more private alternative to clinical testing.

Compared to a traditional blood screening, the saliva test OraQuick HIV1/2, the only oral fluid test approved for use in a health-care setting by the Food and Drug Administration, was 99 percent accurate in detecting HIV antibodies in high-risk populations and about 97 percent in low-risk populations, according to study findings published in the journal The Lancet Infectious Diseases.

To evaluate this saliva test's potential for worldwide use, researchers analyzed real-life field research data from five global databases. High-risk groups include injection drug users, men who have sex with men, and people who have unprotected sex.

Much like home pregnancy tests, researchers believe that oral HIV self-tests can serve as an effective preliminary method of diagnosis.

"Getting people to show up for HIV testing at public clinics has been difficult because of visibility, stigma, lack of privacy and discrimination," the study’s lead author, Dr. Nitika Pant Pai, said in a release announcing the study findings. "A confidential testing option such as self-testing could bring an end to the stigmatization associated with HIV testing."

Earlier this month, another innovative HIV testing program called Testing Together was unveiled, allowing couples to hear their HIV status together, within minutes of receiving a blood test.