HOW CAN THE HIV/AIDS BANDWAGON BE STOPPED?

I’ve been wondering for several years, and I’ve also been asked quite often, “When will HIV/AIDS theory be abandoned? How will that happen?”

According to Yogi Berra, prediction is very hard, especially about the future. The only solid basis for attempting predictions is to extrapolate from the past and present, which can’t take account of the “unknown unknown”—the totally unforeseeable stuff—waiting to trip up even the most judicious and careful projections.

But when it comes to HIV/AIDS, there aren’t even comparable cases from which to extrapolate. Sure enough, plenty of beliefs in science, and a fortiori in medicine, have been found wanting over the centuries, that’s how understanding has advanced; “scientific revolutions” have overturned, displaced, repudiated long-held beliefs—about atoms, about the Earth’s age, about the relation between chemicals in living and non-living entities, about literally innumerable matters.

However, HIV/AIDS isn’t just a belief in medical science, it’s a huge industry, of direct benefit to many groups and to enormous numbers of people at many levels of society and throughout the world (see “Vested Interests”, p. 212 ff. in The Origins, Persistence and Failings of HIV/AIDS Theory). Researchers benefit from expenditures on HIV/AIDS that are 10 to 100 times more per patient or per death than is spent on diabetes or cardiovascular disease (Fair Allocations in Research Foundation) . Africa gets far more for HIV/AIDS-related matters than for anything else; for instance, while researchers in developed countries make a good-enough grant-living from HIV/AIDS, academics and researchers and their assistants in African countries enjoy largesse that others in those countries couldn’t even dream of having. Drug companies make enormous profits. Researchers and drug companies are able to carry out clinical trials in Africa that would never be approved in developed countries (DRUGS OR FOOD?, 25 December 2007; ARE INTESTINAL WORMS GOOD FOR US? ARE THEY GOOD FOR AFRICANS? FOR AFRICAN CHILDREN?, 30 December 2007). Tens of thousands of organizations are involved in HIV/AIDS, and innumerable individuals—very much including so-called activists—make their living from HIV/AIDS-related activities.

Of course, if the scientific community were to proclaim a consensus that HIV doesn’t cause AIDS, others would fall in line. But what might move the scientific community to reach such a consensus? All the funding agencies, all the official institutions international as well as national, all the editors of the most entrenched and prestigious journals and the “peer” reviewers they choose, all the science journalists who have specialized in covering HIV/AIDS, are vested in HIV/AIDS dogma—vested in terms of career, reputation, plain self-interest.

Those are the facts. Documented testimonies are freely available. Scientific papers challenging any aspect of HIV/AIDS dogma are routinely rejected by Nature, Science, Lancet, JAMA, New England Journal of Medicine, etc. “Dissidents” are persecuted shamefully (DISSENTING FROM HIV/AIDS THEORY, 8 December 2007). Thousands of signatories to petitions that HIV/AIDS be rethought understand that they had better keep that belief separate from their work, and some unknown number are even unwilling to have their names publicly known.

So, one cannot reasonably expect that some epidemic of heart-changing by the powers-that-be will transform this situation. If the mainstream scientific consensus is to change, it will have to be pushed by external forces to reconsider the evidence.

This situation prompted me to take special notice of a sentence in a mystery I was reading (Philip Kerr, “The One from the Other”):

“Hard to comprehend, yes. But not so hard to believe.”

The accumulated evidence forces belief, forces one to accept that, indeed, the mainstream medical-scientific community ignores competently presented and substantively supported views that run counter to the contemporary bandwagon. The evidence forces intellectual acceptance of the fact that this is the way things are. But we rebel against that emotionally, because we cannot comprehend, grasp, that medical science is so very different from how we have been conceiving science to be: objective, self-correcting, concerned primarily and only with truth.

That ideal view of science was not obviously misguided up to perhaps the middle of the 20th century, when one could still understand much about scientific activity as the result of an intellectual free market in which individual truth-seekers collaborated and competed. However, roughly since the Second World War, science has increasingly become a matter of knowledge monopolies and research cartels (for a longer discussion, read my essay on 21st-century science).

At a personal level, I find that I cannot comprehend that individuals should be so impervious to evidence or so uninterested in the whole subject. Like other human beings, I tend to judge others by myself. I came to be an HIV skeptic through a particular combination of personal experience and objective evidence. Subsequently, I make naturally the common yet mistaken assumption that others exposed to the same objective evidence would draw the same conclusions. But others don’t have the same background of personal experience that I do, and it is that personal background that explains why I took an interest in the topic in the first place and why I was able to view the evidence in a non-bandwagon manner.

I suggest that I’m fairly typical of HIV/AIDS dissidents in this. Books, articles, blogs, letters to the editor, and more, have been produced by dissidents under the implicit belief that the HIV/AIDS paradigm can be toppled by presenting the evidence against it. We have to comprehend that this is not so.

Certainly it was necessary to make the scientific case. But that has been overwhelming for a long time now, and the question becomes, How can the evidence be used to bring down this bandwagon? What social or political forces can be harnessed that are sufficiently influential to stand against this colossal combination of vested interests? How can those forces be enticed to take a fresh look at beliefs that have become so entrenched? Who would benefit from it?

TUBERCULOSIS AGAIN

Further to IS TUBERCULOSIS AN APHRODISIAC? (4 January 2008):

“Tuberculosis, HIV/AIDS: Twin Harbingers of Death”, 22 January 2008
“Health experts assert that effectively treating tuberculosis will not solve the worldwide HIV/AIDS crisis, but it will significantly reduce its burden. This is the strategy of a local body as it battles these twin agents of death through its health centres scattered throughout Nigeria. Godwin Haruna writes . . .
Tuberculosis (TB) and HIV/AIDS epidemics fuel one another and health experts say they are inextricably linked. According to Dr. Nanshep Daniel Gobgab, director of primary health care system and programmes of the Christian Health Association of Nigeria (CHAN), the weakened immune system of an individual living with HIV increases the likelihood of developing tuberculosis. Gobgab adds that the development of active TB accelerates the progression of HIV disease towards full-blown AIDS.”

It would be uncharitable, of course, to ask for an explanation of the mechanism by which active TB accelerates the progression of HIV disease, if for no other reason than that the mechanism by which HIV causes disease is itself an enduring mystery. Montagnier’s lab showed that, in vitro, CD4 cells are not killed by HIV in the presence of antibiotic, which marks the killer as a microbe and not a virus (Lemaître et al. Research in Virology 141 [1990] 5-16; Infection and Immunity 60 [1992] 742–8). The mainstream has long abandoned the view that HIV kills immune-system cells directly, and a number of suggestions have been made, none of them substantiated to the level of general acceptance: antigenic diversity; super antigen; T-cell anergy; apoptosis; Th1-Th2 switch (Chapter 7, Principles of Molecular Virology).

“ ‘Most TB cases in people with HIV are from reactivation of old infections. However, since tuberculosis is spread by casual contact, people with HIV/AIDS can also contract new or primary TB infection. These new infections can progress rapidly to active disease, rather than follow the typical course of years of dormancy’”

Since “people with HIV/AIDS” means “HIV-positive”, in other words, already exposed to a health challenge of some sort, of course they will be more prone to succumb to some additional health challenge

“TB is the leading killer of people with AIDS. In fact, tuberculosis is the first manifestation of AIDS in over 50 percent of cases in the developing world. According to her, people who are infected with TB and are HIV positive are 3 to 10 times more likely to develop TB than people without HIV infection.”

Exactly. Those TB patients who are HIV-positive are the ones who are more seriously ill. Note that “AIDS” was discovered because people were coming down with opportunistic infections—fungal pneumonia, yeast infections—not with common diseases like TB. AIDS nowadays is an entirely different thing than 1980s AIDS.

“ . . . one-third of HIV-infected people worldwide are co-infected with TB, and TB is responsible for the death of one out of every three people with HIV/AIDS worldwide.”

Exactly. One-third of HIV-positive people are HIV-positive only because they have TB.

“Escalating tuberculosis rates over the past 10 years in many countries, particularly in sub-Saharan Africa and parts of Southeast Asia are largely attributable to the HIV/AIDS epidemic.”

The so-called AIDS epidemic in Africa and Asia is largely a TB epidemic.

“Much of TB’s resurgence is directly connected to the explosive spread of HIV, especially in Africa, where two-thirds of HIV patients carry tuberculosis.”

But there hasn’t been an explosive spread of HIV. Its prevalence has remained the same in every region for which UNAIDS and CDC have been giving estimates; see for example Preface, Figure 26, and Tables 20 & 31 in The Origins, Persistence and Failings of HIV/AIDS Theory (McFarland 2007).

Activists don’t hesitate to use the supposed connection between TB and HIV/AIDS to their own advantage, of course:

“Campaigners against TB and AIDS Urged to Co-operate”, by Miriam Mannak (10 November 2007)
“Tuberculosis (TB) in Africa cannot be dealt with while TB and HIV/AIDS organisations refuse to set aside their differences, health experts said Friday during the 38th Union World Conference on Lung Health. ‘So far, many TB and HIV programmes in Africa—or anywhere in the world—do not co-operate with one another, despite the strong connection that exists between HIV and TB’ . . . . ‘In some African countries for instance, 75 percent to 80 percent of the people living with TB are co-infected with HIV’”

Again: TB is one of the conditions that can cause a positive HIV-test

“HIV has always been the big kid on the block, with TB being the little brother. HIV programmes and organisations seem to be afraid that TB takes away attention and funding.”

Of course; that’s what it’s all about, who gets the money.

“ ‘In 2005, only seven percent of HIV patients worldwide were tested for TB,’ said Alasdair Reid, HIV/TB advisor to the Joint United Nations Programme on HIV/AIDS. ‘That is shocking. By testing people living with HIV for TB we can save thousands and thousands of lives each year. And, it is feasible. The problem is the lack of co-operation between the different organisations that deal with TB or HIV.’ new model for distribution of funds is also required, Reid added. “Currently, money is raised for either HIV or TB, and funds dedicated for HIV can’t be used for TB or vice versa.’”

Exactly; it’s all about who gets the money. And these officials don’t hesitate to talk utter rubbish:

“When you want to tackle HIV you need to tackle TB, especially in Africa where so many people are co-infected.”

REINFORCING THE DOGMA

Happened to come across a schedule of “HIV/AIDS Events” in Lousiville KY in 2008 (Metro Calendar):

February 7, 2008:   National Black HIV/AIDS Awareness Day
March 2- 9, 2008:   HIV/AIDS Black Church Week of Prayer
June 27, 2008:   National HIV Testing Day
September 28, 2008:   Louisville AIDS Walk
October 15, 2008:   National Latino AIDS Awareness Day
December 1, 2008:   World AIDS Day

The difficulty that dissidents have in getting uninformed (that is, indoctrinated) people to pay attention to the evidence is underscored by the fact that there are so many similar happenings around the world, with public hooplah, celebrity appearances, and heart-string-pulling anecdotes and pictures.

**********************

In Africa, HIV/AIDS dogma is reinforced because so much foreign aid supports HIV/AIDS-related activities. The Krynens, French social workers in Africa, discovered that large numbers of “AIDS orphans” are simply children whose parents leave them—often only seasonally—with grandparents or others while the parents go to where they can find work; read Neville Hodgkinson’s splendid “AIDS—The failure of contemporary science: How a virus that never was deceived the world” (Fourth Estate, 1996)—it’s out of print, but can be found at http://www.abebooks.com/.

In that light, consider the following news item:

“HIV orphans’ custodians get upkeep funds (24 January 2008, Kenya DAILY NATION):
The Government Wednesday paid out Sh 2.5 million to caretakers of orphans in Kirinyaga district. . . . 250 custodians had received the funds. The money is to help beneficiaries provide upkeep for the orphans who are Hiv/Aids victims.
. . . . The programme which was launched last year sees each caretaker getting Sh1,500 on a monthly basis.”

One wonders what other sources of income those caretakers have, and how likely they might be to say anything that could threaten continuation of this largesse.

HIV “INFECTION” DISAPPEARS SPONTANEOUSLY

HIV/AIDS dogma has it that there’s no cure; once infected by HIV—as demonstrated for example by confirmed positive HIV-antibody tests—there’s no possibility of reversion to uninfected, not even by antiretroviral treatment. The long-term healthy “non-progressors” or “elite controllers” still remain infected, they just have some mysterious physiological knack that stops illness from developing.

Dissidents know different. The epidemiology of HIV in the United States shows that testing HIV-positive is not the mark of an infection, it’s a quite non-specific reaction (The Origins, Persistence and Failings of HIV/AIDS Theory); according to the Perth Group, a sign of oxidative stress.

The latter view explains why HIV-positive people can and sometimes do spontaneously revert to HIV-negative, illustrations of which are cited at p. 96 ff., “HIV-positive may be only temporary”, in The Origins, Persistence and Failings of HIV/AIDS Theory.

The orthodoxy has ignored this evidence that HIV-positive may be temporary, so it’s something of a surprise to see published in a mainstream journal the report of “Spontaneous HIV-1 seroreversion in an adult male” (Coyne et al., Sexually Transmitted Diseases, 34 [2007] 627-30). That article is well worth having in one’s files, for several reasons:

— The man in question is in a high-risk group, he is a young gay man.

— The meticulous series of tests carried out by Coyne et al. gave results precisely in accord with what the orthodoxy postulates for a newly infected person: negative HIV tests, risky behavior, an episode of “gastro-intestinal symptoms, sweats, rash, and lymphadenopathy”, followed by inconclusive tests, followed finally by positive tests. “This man was at high risk of HIV acquisition and had symptoms consistent with HIV seroconversion. His HIV antibody response evolved from negative to equivocal to a combination of reactions considered to be positive, and the interpretation was that he had developed HIV infection.”

— The researchers used a stunning array of tests from a variety of manufacturers. The implicit inference from the use of so many tests is that any given test kit is unreliable; and the data support that inference. For example (their Table 1), on the same day one test is negative, p24 antigen also negative, yet another test is positive. A few weeks later, again one positive and another negative.

— Positive antibody tests are supposed to run parallel with appreciable viral load. “However, persistently undetectable viral loads prompted repeat antibody tests 10 months later, which were negative. P24 antigen and proviral DNA could not be detected. . . . Our patient did not have immunosuppression or antiretroviral drugs to account for his seroreversion. Nor did he have detectable proviral DNA to indicate he was infected with HIV. His results are therefore intriguing.”

The authors mention the possibilities of non-specific reactions and false positives, but in so dismissive a manner as to effectively discount them—“These findings appear to be exceptionally rare”.

They would have liked to study this case further “if the patient had consented to further investigations”. I’m inclined to be on his side in refusing. Having been told of being infected by a fatal, incurable, disease, he was subjected to innumerable tests; then, after months of undoubted mental anguish, he was told by obviously puzzled doctors that they really didn’t understand what was going on, but that apparently he might not be incurably ill after all, they had possibly frightened him for no good reason—but of course they couldn’t be sure, they’d love to keep on doing tests (maybe in the hope that he’d turn out to be fatally ill after all?).

* * * * * *

Coyne et al. sum up their paper with “These findings appear to be exceptionally rare”. That displays a highly selective point of view, for the literature is replete with data showing that the tests are unreliable, that seroreversions occur quite often, that CD4 counts do not jibe with viral load, and that neither viral load nor CD4 counts jibe with patient health.

This paper has five authors, who are associated with organizations in the United Kingdom specializing in HIV, infections in general, and virology. It reveals something about contemporary medical science that the flood of HIV-related publications persistently ignore even mainstream publications that fail to support the prevailing dogma, for example, that babies spontaneously revert from HIV-positive to HIV-negative (Clinical and Experimental Immunology 102: 476, Lancet 347: 213, New England Journal of Medicine 332: 833) and that drug abusers also revert spontaneously if they kick the habit and that needle-sharing is NOT associated with higher “infection rates” (American Journal of Epidemiology 146: 994); that HAART doesn’t work (Lancet 368: 451), that “viral isolates” are mixtures (Virology 230: 134), that sexual transmission cannot explain the African “AIDS epidemic” (AIDS 4: 11, International Journal of STD & AIDS 14: 144); and much more.

TO AVOID HIV LATER, DAMAGE YOUR KIDNEYS AND LIVER NOW

Clinical trials on human beings are under way to gauge how well tenofovir and emtricitabine protect against HIV infection, with the hope that a regular diet of them could be recommended as prophylaxis.

It’s already known, mind you, that these drugs can produce bone demineralization with chronic use, kidney damage, lactic acidosis (including fatalities), liver damage (including fatalities), and liver cancer. The danger of side effects is greatest when first starting the drugs but also when one stops taking them.

The brilliant idea that this may be useful prophylaxis is based on studies in “humanized” mice—FIVE mice, that is—engineered to have a “human-type” immune system. The media (http://cbs11tv.com/local/HIV.Transmission.Prevention.2.631367.html) help everyone understand how significant this is by pointing out that “Humanized mice . . . have the same immune systems and infection fighting cells as humans”; which could make one wonder why there’s even a need for trials in actual human beings.

The concept of prophylaxis using drugs that treat the actual illness is in itself a remarkable advance. Perhaps instead of exposing babies to the dangers of vaccination, we should simply place them on life-long diets of antibiotics? Come to think of it, we do already practice this sort of prophylaxis by feeding antiretroviral drugs to every available pregnant woman who happens to be HIV-positive—see FIRST: DO NO HARM! (19 December 2007).

As to humanizing mice, I’m sorely tempted to speculate about the possibility of engineering mice to have human-type intelligence—sufficient, at the very least, for carrying on HIV/AIDS research and clinical trials.

* * * * * *

Here is what the Official Treatment Guidelines, December 2007 version, say about the side effects of tenofovir and emtricitabine, which are described in the media story below as “fewer . . . than other HIV treatments”:

“Renal impairment, manifested by increases in serum creatinine, glycosuria, hypophosphatemia, and acute tubular necrosis, has been reported with tenofovir use [152, 153]. The extent of this toxicity is still undefined. . . .
. . . .
Discontinuation of emtricitabine, lamivudine, or tenofovir in patients with hepatitis B coinfection. Patients with hepatitis B coinfection (hepatitis B surface antigen or HBeAg positive) and receiving one or a combination of these NRTIs may experience an exacerbation of hepatitis upon drug discontinuation [164, 165]. If any of the above agents is discontinued, the patients should be closely monitored for exacerbation of hepatitis or for hepatic flare (AII).
. . . .
Need to discontinue emtricitabine, lamivudine, or tenofovir: Monitor clinical course with frequent liver function tests, and consider the use of interferon, adefovir dipivoxil, or telbivudine to prevent flares, especially in patients with marginal hepatic reserve.
. . . .
Pertinent Black Box Warning Information:
Emtricitabine (EMTRIVA); or in combination product with tenofovir DF (TRUVADA) or with tenofovir DF and efavirenz (ATRIPLA):
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues alone or in combination with other antiretrovirals.
—Emtricitabine is not indicated for the treatment of hepatitis B infection (HBV), the safety and efficacy have not been established in patients with HIV/HBV coinfection.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued emtricitabine – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Tenofovir (VIREAD); or in combination product with emtricitabine (TRUVADA) or with efavirenz and emtricitabine (ATRIPLA)
—Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogs alone or in combination with other antiretrovirals.
—Tenofovir is not indicated for the treatment of chronic hepatitis B (HBV) infection, safety and efficacy in patients with HIV/HBV coinfection have not been established.
—Severe acute exacerbations of hepatitis B have been reported in patients who discontinued tenofovir – hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months after discontinuation of tenofovir in HIV/HBV coinfected patients.
—If appropriate, initiation of anti-HBV therapy may be warranted after discontinuation of tenofovir.
. . . .
Studies in monkeys show decreased fetal growth and reduction in fetal bone porosity within two months of starting maternal therapy [371]. Clinical studies in humans (particularly children) show bone demineralization with chronic use; clinical significance unknown [252, 372]. Significant placental passage in humans (cord:maternal blood ratio ~1.0).”

Tenofovir also produces liver cancer in mice.

* * * * * *

Here’s the media report of this study:

“After 25 years of researchers around the globe being confounded by HIV, scientists in Dallas have shown that the virus’s transmission can be stopped with medications. The scientific first, though performed only in lab mice, bodes well for a future when people at high risk for HIV infection would have a convenient way to protect themselves from the virus. . . . experts who have long advocated safe-sex practices are worried that people will seek these drugs without waiting for scientific proof from human studies. . . . One of the drugs, tenofovir, is reportedly being sold at gay dance clubs on both coasts as a protection against HIV. . . .
Someday, people at high risk of HIV infection could be encouraged by doctors to take a daily pill . . . .
The experiment involved injecting five mice for seven days with two drugs that are commonly used to treat AIDS patients, tenofovir and emtricitabine. On the third day, the mice were inoculated vaginally with HIV, to mimic how most women and girls become infected. ‘Women have no way of protecting themselves from … [sexually transmitted diseases] and HIV,’ said Dr. Garcia, a professor of internal medicine. A preventive medication ‘would empower them to at least have a fighting chance.’ . . .
An important step toward the current UT Southwestern study was Dr. Garcia’s 2006 development of a mouse that had been made susceptible to HIV via transplantation of a ‘humanized’ immune system’. . . .
The two [drugs] . . . have fewer side effects than other HIV treatments. The two drugs are part of several studies in people, funded by the U.S. government, that are testing safety and effectiveness in preventing HIV infection among intravenous drug abusers, young men and women who are sexually active and men who have sex with men. Test sites include San Francisco, Atlanta, Botswana, Thailand, Peru and Ecuador” [emphases added].
(“Dallas scientists stop HIV from spreading in mice—Experts caution that Dallas team’s findings were only in mice”, by Sue Goetinck Ambrose & Sherry Jacobson , Dallas Morning News, 15 January 2008).
The source article is “Antiretroviral pre-exposure prophylaxis prevents vaginal transmission of HIV-1 in humanized BLT mice” by Denton et al., PLoS Medicine 5 #1, e16 doi:10.1371/journal.pmed.0050016 in PLoS Medicine