HIV/AIDS Skepticism

Pointing to evidence that HIV is not the necessary and sufficient cause of AIDS

Archive for August, 2008

CRACK COCAINE CAUSES AIDS!

Posted by Henry Bauer on 2008/08/12

Peter Duesberg has adduced much evidence supporting the claim that abuse of recreational drugs can cause “AIDS”. Gordon Stewart noted “AIDS”-like symptoms in drug abusers before the AIDS era (p. 103f. in Hodgkinson, “AIDS; The Failure of Contemporary Science” ). A recent publication confirms that crack cocaine can cause AIDS:

“Persistent crack users were over three times as likely as non-users to die from AIDS-related causes, controlling for use of HAART self-reported at 95% or higher adherence, problem drinking, age, race, income, education, illness duration, study site, and baseline virologic and immunologic indicators. Persistent crack users and intermittent users in active and abstinent phases showed greater CD4 cell loss and higher HIV-1 RNA levels controlling for the same covariates. Persistent and intermittent crack users were more likely than non-users to develop new AIDS-defining illnesses controlling for identical confounds. These results persisted when controlling for heroin use, tobacco smoking, depressive symptoms, hepatitis C virus coinfection, and injection drug use. CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women” (Cook et al., “Crack cocaine, disease progression, and mortality in a multicenter cohort of HIV-1 positive women”, AIDS 22 [2008] 1355-63 ).

Of course the authors of this study don’t admit that it is the cocaine that causes the “HIV-1 disease progression” and “AIDS-related mortality”; they interpret the results as signifying that crack cocaine somehow enhances the evil effects of HIV.

Cook et al. controlled, commendably, for many conceivably confounding variables: heroin use, tobacco smoking, depressive symptoms, hepatitis C virus co-infection, injection drug use (crack cocaine is smoked, not injected). But they failed to control for the single most centrally relevant variable: “HIV-positive”. What would have been the findings had the comparison been between crack users who are HIV-negative and others who are “HIV-positive”?

But, of course, such controls might be very difficult to find, especially with comparable levels of drug intake, because drug abusers test “HIV-positive” as frequently as do TB patients and fast-lane gay men:

Whatever it is that stimulates an “HIV-positive” response–or rather, whatever “they” are, whatever range of molecular species it is that can produce an “HIV-positive” response–, evidently most or all “recreational” drugs are capable of doing so, as well as of causing illnesses that could be called “AIDS”.

Everything in this article by Cook et al., and in other literature cited there, is readily explained on the basis that crack cocaine and other drugs produce an “HIV-positive” response, ill health in general, and specific damage to the immune system. Cocaine has been shown to cause “immune alterations”, “decreasing operation of important immune responses”. It causes “membrane permeability” permitting passage across the “blood-brain barrier”—recall Tony Lance’s report (gay-related-intestinal-dysbiosis.pdf) that “leaky gut syndrome” seems able to produce an “HIV-positive” response as well as illness [WHAT REALLY CAUSED AIDS: SLICING THROUGH THE GORDIAN KNOT, 20 February 2008]. Cocaine has been shown to interfere specifically with the Th1-Th2 balance that seems involved in “HIV-positive” and in AIDS [Culshaw, Journal of American Physicians and Surgeons 11 (#4, Winter 2006) 101-5; Sacher, AIDS AS INTESTINAL DYSBIOSIS, 23 February 2008, and ALTERNATIVE TREATMENTS FOR AIDS, 25 February 2008]. One cited study had already reported crack use as stimulating progression to AIDS. Another study had found “the risk of AIDS-related opportunistic conditions was greater for persistent users  and intermittent  users  during periods of active use, with no difference during periods of abstinence” [emphasis added], consistent with reports that HIV-positive drug abusers revert to HIV-negative when they abstain (Moss et al., AIDS 8 (1994) 223–31). The cited finding that “hard drug use (i.e., cocaine, heroin, methadone, or injection drugs) was significantly associated with AIDS-defining illnesses, but not with change in CD4 cell count, HIV- RNA, or mortality” is consistent with the finding that CD4 counts, viral load, and clinical progression are not directly correlated (Rodriguez et al., JAMA 296 [2006] 1498-1506). The cited fact from another study that “cocaine in combination with alcohol places individuals at increased risk of infection with a number of pathogens, due to additive or synergistic effects resulting in impaired immune function” will seem surprising only to people unaware that alcohol and cocaine are both bad for health.

Despite all the previous work referred to, despite the sheer common-sense knowledge that drugs are bad for you [COCAINE AND HEROIN AREN’T GOOD FOR YOU! — a Golden Fleece Award, 13 June 2008], the authors congratulate themselves on the ground-breaking nature of their work: “Ours is the first study to show that use of crack cocaine in a  large,  national  cohort  of  HIV-positive  women  is longitudinally associated with subsequent deterioration in immune status, failure of virologic suppression, development of AIDS-defining conditions, and mortality due to AIDS-related causes, even among those who reported adhering to HAART regimens 95% of the time or more”.

Ample grounds for seeking research grants to take this knowledge even further.

Posted in experts, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV tests | Tagged: , , , , , , , , , , , , , , | 24 Comments »

Measuring VIRAL LOAD WITHOUT VIRUS: Where are the virions?

Posted by Henry Bauer on 2008/08/10

A continuing puzzle, at least for this lay person, is why HIV/AIDS researchers have never bothered to extract virions—whole particles of HIV—from HIV-positive people or from AIDS patients. Soon after “infection”, after all, the former are supposed to be teeming with virus, and AIDS victims are supposed to be full of virus (again) by the time opportunistic infections get a foothold; according to Fauci et al., there are then about 1,000,000 million and 100,000 “HIV RNA copies”, respectively, in each milliliter of plasma, each copy supposedly representing a virion:

Since primary infection and “acute viral syndrome” are often unaccompanied by any clinical symptoms—at best (or worst) mild flu-like signs or rashes—I had long thought that it would be unfair to chide mainstream researchers for failing to extract genuine virus at that stage. But, it turns out, some researchers have been able to carry out sophisticated studies of blood drawn during those critical initial weeks of primary infection.

Gasper-Smith et al. report on “Induction of plasma (TRAIL), TNFR-2, Fas ligand, and plasma microparticles after Human Immunodeficiency Virus Type 1 (HIV-1) transmission: Implications for HIV-1 vaccine design”, Journal of Virology 82 [2008] 7700-10. They conclude that “Release of products of cell death and subsequent immunosuppression following HIV-1 transmission could potentially narrow the window of opportunity during which a vaccine is able to extinguish HIV-1 infection and could place severe constraints on the amount of time available for the immune system to respond to the transmitted virus”.

The researchers had been able to obtain from ZeptoMetrix Corporation of Buffalo (NY) “seroconversion panels” consisting of “sequential aliquots of plasma (range, 4 to 30 aliquots) collected approximately every 3 days during the time of acute infection with HIV-1”; they cite, for the availability of these seroconversion panels, Fiebig et al., “Dynamics of HIV viremia and antibody seroconversion in plasma donors: Implications for diagnosis and staging of primary HIV infection” , AIDS 17 [2003] 1871-9.

Here, it seemed to me, had been an ideal opportunity to extract veritable whole particles of HIV generated during the acute initial infection. But the only mention of “virion” in the Gasper-Smith article is in this sentence: “While the average peak HIV-1 VL level was 1,421,628 copies/ ml, the average total MP peak level was 606,881,733/ml. Thus, at the times of maximum VL and MP levels, the average number of MPs was 427 times larger than the average number of virions”. “VL” of course is viral load. “MP” is not military police (or, as Lucas reminded me, Members of Parliament), it is “microparticles”:

“MPs are small membrane-bound vesicles that are released from the surface of apoptotic cells by exocytic or budding processes; . . . . MPs, which circulate in the blood under many clinical conditions, are part of a spectrum of subcellular structures that are released from cells and can be distinguished from exosomes . . . . MPs have immunomodulatory activities and can promote immune cell death; exosomes are also immunologically active, can suppress immune responses . . . , and have been reported to have been found at elevated levels in cases of chronic HIV-1 infection . . . . If elevations in levels of immunosuppressive molecules, coupled with early CD4+ T-cell death, occur early following HIV-1 transmission, then these events could potentially define a protected time during which HIV-1 is able to replicate while anti-HIV-1 T- or B-cell responses are suppressed” [emphases added].

Gasper-Smith et al. counted and extracted and studied the MPs by flow cytometry and electron microscopy. Why did they not also study HIV particles? Did the freezing and storing of the plasma destroy HIV virions while leaving MPs intact?

There were 427 times as many MPs as copies of RNA supposed to stem from HIV. MPs can “promote immune cell death”. How do we know that the CD4 cells supposedly killed by HIV weren’t killed by the MPs?

Though phrased rhetorically and left unanswered, I intend those questions to be taken quite seriously. If I wanted to be flippant or sarcastic, I might have commented once again on the peculiar penchant among HIV/AIDS researchers to imply that their measurements are accurate to an impossible number of significant figures when they report MPs of “606,881,733/ml”. That’s one of the drawbacks of the digital age, I suppose. In the good old days when we read measurements off scales with pointers, we weren’t tempted to write down meaningless numbers.

Perhaps Fiebig et al., cited by Gasper-Smith et al. for the brilliant idea of getting those stored samples from blood donors, had looked for whole particles of HIV?

“Because of the difficulty in obtaining blood samples representing early acute HIV infection from clinical patients, most patients do not come to medical attention until weeks to months after infection, we resorted to stored, frozen plasma collections from plasma donors, who unrelated to donating became infected with HIV, and were deferred from further donating. As plasma donors donate on average twice a week, and every donation is tested for HIV and held for 60 days before release, their archived samples provide a unique record of the infection from timepoints before viral exposure until seroconversion and beyond. . . . Plasma donations (600-800 ml) from source plasma donors were routinely collected at approximately twice weekly intervals and stored frozen at -20oC or less.”

Plenty of material to work with, it would seem—600 ml is well over a pint, and ought to contain many millions of HIV virions, at “1,421,628” per ml.

But, NO. In the Fiebig article, there’s not a single mention of “virion”. They used ELISA, p24 antigen, and HIV-1-RNA tests to determine how much “HIV” was present.

—————————

Is the failure to even try to extract virions somehow related to the fact that Gallo was more often able to “isolate” HIV from “pre-AIDS” patients than from those who actually had AIDS? Here’s from the Abstract of Gallo’s ground-breaking article that followed the press conference announcing discovery of the probable cause of AIDS:

“Peripheral blood lymphocytes from patients with the acquired immunodeficiency syndrome (AIDS) or with signs or symptoms that frequently precede AIDS (pre-AIDS) were grown in vitro with added T-cell growth factor and assayed for the expression and release of human T-lymphotropic retroviruses (HTLV)” (Gallo et al., Science 224 [1984] 500-3).

That’s what Gallo means by “isolation”, as other rethinkers have often remarked. It’s not the commonly used meaning of the word, namely, “extraction” or “separation from”. And it’s not as though the “assaying” involved separating virions from those cultures, either.

“Retroviruses . . . were isolated from a total of 48 subjects including 18 of 21 patients with pre-AIDS, three of four clinically normal mothers of juveniles with AIDS, 26 of 72 adult and juvenile patients with AIDS, and from one of 22 normal male homosexual subjects”.

Why from more pre-AIDS than from actual AIDS patients?

The Abstract ends with “These results and those reported elsewhere in this issue suggest that HTLV-III may be the primary cause of AIDS” [emphases added].

From that modest suggestion, the dogma that HIV causes AIDS evolved without the benefit of direct isolation—extraction, separation—of whole infectious virions from even a single HIV-positive or AIDS-suffering person, or from plasma preserved from periods of “acute viral syndrome”.

Posted in HIV skepticism, HIV/AIDS numbers | Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , | 9 Comments »

NEVIRAPINE — P.S.

Posted by Henry Bauer on 2008/08/06

No sooner had we posted about the toxicity of nevirapine than it was featured in another story:
Stanford Study Finds HIV Drug Can Persist in Mothers’ Milk, Increasing Risk to Them and Their Babies” (SOURCE: Stanford University Medical Center)

“STANFORD, Calif., Aug 05, 2008 (BUSINESS WIRE) — A drug commonly used in the developing world to prevent transmission of HIV from mother to child persists in the breast milk and blood of the mothers, putting them and their babies at risk for developing drug-resistant strains of the virus, according to researchers at the Stanford University School of Medicine” [emphasis added].

Over and over again, HIV/AIDS researchers show that the only thing they care about is THE VIRUS.

God forbid that THE VIRUS should escape our drugs! If we have to ruin the livers of mothers and babies in order to kill the virus—well, that’s unavoidable collateral damage. What’s intolerable is that the drugs should be so ineffective as to allow mutant strains of THE VIRUS to evolve.

“The researchers found that the drug, nevirapine, stays in the blood and breast milk of the infected mothers for at least two weeks. During that time, the virus has ample opportunity to transform itself into drug-resistant strains of HIV, the human immunodeficiency virus that causes AIDS, which can be very difficult to treat.”

What about the hepatotoxicity? What happens to the livers of those newborns during those two weeks?

“In the short term, nevirapine is better than nothing,” said David Katzenstein, MD, professor of infectious diseases and principal investigator of the study. [Some might argue, on rather solid grounds, that “nothing”—doing nothing— would actually be much better than nevirapine.]  “But in the long term, I’m concerned about conferring resistance. If you’re talking about resistance on a broad scale, it could jeopardize future treatment for mothers and infants” [assuming, of course, that in the meantime they haven’t succumbed to liver failure or other “side”-effects of antiretroviral drugs].

“Seble Kassaye, MD, instructor in infectious diseases and first author of the study, will present the results Aug. 5 at the International AIDS Conference in Mexico City”
where many other studies will also be presented in which THE VIRUS is the focus, not the quality of life of people who happen to test “HIV-positive”.

As is characteristic of the HIV/AIDS scene, facts are ignored in favor of shibboleths and myths:
“Sixty-five percent [of the mothers] had drug-resistant strains in their breast milk as well, with the potential to pass this on to their babies through breastfeeding, a common mode of viral transmission”.
But study after study has shown that the more there is breast-feeding, the LESS likely that the baby becomes “HIV-positive” [MORE HIV, LESS INFECTION: THE BREASTFEEDING CONUNDRUM, 21 November; HIV and BREASTFEEDING AGAIN, 13 February 2008].

“Last year, 420,000 babies were born HIV-positive, the large majority of them to HIV-infected mothers in sub-Saharan Africa, according to figures from the United Nations Joint Programme on HIV/AIDS. The centerpiece of public health programs in the developing world to stop mother-to-child transmission of HIV are both zidovudine (AZT) and nevirapine, which have been used as preventive tools in nearly 900,000 women and infants worldwide”.
Several of my posts have addressed the question, how can the HIV/AIDS bandwagon be stopped? [HOW CAN THE HIV/AIDS BANDWAGON BE STOPPED?, 27 January 2008; STOPPING THE HIV/AIDS BANDWAGON—-Part II, 1 February 2008; A SMALL HITCH IN THE BANDWAGON?, 29 May 2008; The CASES AGAINST HIV: Strategies for Halting the Bandwagon, 29 July 2008].

Here’s one unpleasant possibility. AZT and nevirapine continue to be administered to increasing numbers of African women and babies. Over time, the liver damage to mothers and babies and life-long mitochondrial damage to the babies become so obvious that they can no longer be ignored.

To coin a phrase, there will then be hell to pay.

Posted in antiretroviral drugs, clinical trials, experts, HIV in children, HIV transmission | Tagged: | 1 Comment »

NEVIRAPINE, TB, and HIV/AIDS

Posted by Henry Bauer on 2008/08/06

TB hampers HIV treatment — study
Patients being treated for tuberculosis (TB) may not get the full benefits from HIV therapy, researchers say. Nevirapine — a cheap antiretroviral drug used to treat HIV in developing countries — did not work as well in patients also on TB treatment. . . . Around 40% of HIV patients in the South African study were also treated for TB. . . . Nevirapine is a common choice because of its cost and can be used in women of child-bearing age.”

That TB patients test HIV-positive at a very high rate has been known for a long time, from data gathered in the United States:

Are TB patients particularly promiscuous sexually, or incessantly sharing infected needles for drug abuse? [IS TUBERCULOSIS AN APHRODISIAC?, 4 January 2008] Or is it that HIV tests, which react “positive” on a wide range of conditions, are particularly prone to test positive in the presence of TB? Surely the latter interpretation is much the more plausible.

As to the benefits of nevirapine and its utility in pregnant women, read Celia Farber’s “Out of Control” [Harper’s magazine, March 2006]: a pregnant woman taking nevirapine in a clinical trial died thereby; and the main initial trial of the drug in Africa had been so flawed that the claims based on it should have been disregarded.

Nevirapine is a known cause of liver disease, sometimes fatal, as well as of other potentially fatal “side”-effects. The following quotes are taken from the January 2008 revision of the official HIV/AIDS treatment guidelines:

“Nevirapine may be used as an alternative to efavirenz for the initial NNRTI-based regimen in women with pretreatment CD4 counts <250 cells/mm3 or in men with pretreatment CD4 counts <400 cells/mm3 (BII). Symptomatic and sometimes serious or life-threatening hepatic events have been observed with much greater frequency in women with pretreatment CD4 counts >250/mm3 and in men with pretreatment CD4 counts >400/mm3. Nevirapine thus should be initiated in these patients only if the benefit clearly outweighs the risk. Close monitoring for elevated liver enzymes and skin rash should be undertaken for all patients during the first 18 weeks of nevirapine therapy. . . . nevirapine was associated with greater toxicity (see below) and did not meet criteria for non-inferiority compared with efavirenz. . . . Two deaths were attributed to nevirapine use. One resulted from fulminant hepatitis and one from staphylococcal sepsis as a complication of Stevens-Johnson syndrome (pp. 18-19).”
“Serious hepatic events have been observed when nevirapine was initiated in treatment-naïve patients. These events generally occur within the first few weeks of treatment. In addition to experiencing elevated serum transaminases, approximately half of the patients also develop skin rash, with or without fever or flu-like symptoms. . . . A 12-fold higher incidence of symptomatic hepatic events was seen in women (including pregnant women) with CD4 counts >250 cells/mm3 at the time of nevirapine initiation . . . . Most of these patients had no identifiable underlying hepatic abnormalities. In some cases, hepatic injuries continued to progress despite discontinuation of nevirapine [129, 131]. . . . More detailed recommendations on the management of nevirapine-associated hepatic events can be found in Table 18a [whose heading is, ‘Potentially Life-Threatening and Serious Adverse Events’] (p. 19).”
“female patients seem to have a higher propensity of developing Stevens-Johnson syndrome and symptomatic hepatic events from nevirapine (p.29).”
“Because nevirapine is an inducer of the drug-metabolizing hepatic enzymes, administration of full therapeutic doses of nevirapine without a 2-week, low-dose escalation phase will result in excess plasma drug levels and potentially increase the risk for toxicity (p. 41).”
“. . . . Hepatic failure and death have been reported among a small number of pregnant patients (p. 48).”
“DISADVANTAGES (Table 9):
• Higher incidence of rash than with other NNRTIs, including rare but serious hypersensitivity reactions (Stevens-Johnson syndrome or toxic epidermal necrolysis)
• Higher incidence of hepatotoxicity than with other NNRTIs, including serious and even fatal cases of hepatic necrosis”

There is also a “Black Box Warning” for nevirapine (Table 20, p. 86):
“• Severe, life-threatening, and in some cases fatal hepatotoxicity, including fulminant and cholestatic hepatitis, hepatic necrosis, and hepatic failure, has been reported. Patients may present with nonspecific prodromes of hepatitis and progress to hepatic failure.
• Women with CD4 counts >250 cells/mm3, including pregnant women receiving chronic treatment for HIV infection, are at considerably higher risk of hepatotoxicities.
• Severe, life-threatening, and even fatal skin reactions, including Stevens-Johnson syndrome, toxic epidermal necrolysis, and hypersensitivity reactions characterized by rash, constitutional findings, and organ dysfunction have occurred with nevirapine treatment.
• Patients should be monitored intensively during the first 18 weeks of nevirapine therapy to detect potentially life-threatening hepatotoxicity or skin reactions.
• A 14-day lead-in period with nevirapine 200 mg daily must be followed strictly.
• Nevirapine should not be restarted after severe hepatic, skin, or hypersensitivity reactions”

“Nevirapine has also been shown in animal studies to cause cancer: “hepatocellular adenomas and carcinomas in mice and rats” (Table 26).”

THAT’s the drug that HIV/AIDS experts describe as “can be used in women of child-bearing age”.
THAT’s the drug widely used in Africa to supposedly protect newborn babies from their “HIV-positive” mothers.

Posted in antiretroviral drugs, clinical trials, experts, HIV tests | Tagged: , , , | 1 Comment »

The EXPERT SPEAKS about AIDS and sexual behavior

Posted by Henry Bauer on 2008/08/06

I hope this won’t seem inappropriate here.

On the morning news I heard  a news report from the 17th International AIDS Conference that brought me up short, wondering whether I could have heard incorrectly.

An expert was saying that the only way to stop AIDS in Africa was for Africans to learn that they had to control and change their sexual behavior.

The expert was former US President Bill Clinton.

He should certainly know quite a lot about that.

Posted in experts, sexual transmission | Tagged: , , , | 2 Comments »