TELLING TRUE STORIES ABOUT HIV/AIDS

How to entice into “rethinking AIDS”, into questioning the conventional wisdom, people who have been thoroughly brainwashed by the constant repetition of “HIV, the virus that causes AIDS”?

A large part of the problem is that the rethinkers’ case is not readily made in a convincing way via self-evident sound-bites. “The ‘HIV’ tests don’t detect a virus”, or “ ‘HIV’ tests have never been proven to be specific for ‘HIV’”, while perfectly true, are based on evidence that is too technical for most people to feel comfortable with; to appreciate the strength of the case against HIV/AIDS theory, to appreciate that those mainstream-contradicting sound-bites are really true, requires prolonged immersion in much data. Even the most concise as well as documented overview, say, Christine Maggiore’s excellent What If Everything You Thought You Knew About AIDS Was Wrong?, or Rebecca Culshaw’s similarly concise yet also comprehensive Science Sold Out: Does HIV Really Cause AIDS?, are hardly bed-time reading. A promising alternative approach is through “fiction”.

There’s a long and respectable history of literary fiction that aims to acquaint readers with important facts. (Most good literature teaches at least indirectly about people and about human life, of course, but I’m now referring to deliberately didactic treatments of specific issues.) Sinclair Lewis in Martin Arrowsmith conveyed important truths about medical practice and medical research and commercial conflicts of interest. Upton Sinclair revealed through novels some ugly truths about the meat-packing industry (The Jungle), the oil industry (Oil), and others, and his Lanny Budd series can serve as a descriptive political history of the era of Nazism, the Second World War, and its aftermath. Most recently, Michael Crichton exposed the lacunae and fault lines in the current obsession with man-caused global warming in State of Fear.

HIV/AIDS seems a natural candidate for this sort of treatment, and Stephen Davis has put his hand, head, and heart into the endeavor. His first novel, Wrongful Death: The AIDS Trial, was published in 2006; the second, Are You Positive?, appeared this year.

Both books feature legal trials, and are thereby consistent with my growing suspicion that HIV/AIDS theory will only be overturned when the mainstream is forced, in a court of law, to reveal the extent to which the theory is like an Emperor wearing no clothes at all.

Wrongful Death tells the story of a class-action suit brought by relatives of those who died needlessly because “HIV-positive” people were treated with AZT. The novel was exceptionally timely, given that the Centers for Disease Control and Prevention was just then recommending that “HIV”-testing should become routine. If that were to happen, then a few perfectly healthy people in every thousand would be misguidedly told that they harbor a deadly virus and should begin taking drugs whose “side” effects make the rate of “adherence to treatment” quite low and which ultimately reward compliant adherence with serious illness and often death.

Davis follows, for legal reasons, the convention of claiming fictional character for the protagonists (except for a few well-known public figures), but readers at all familiar with HIV/AIDS matters will recognize many of the characters, most of whose names are faithful to the initials of their real-life models. The story is told in quite a straightforward manner, an appropriate vehicle for acquainting readers with the facts in a steady succession of digestible pieces. Though the story is straightforwardly told, there are also a couple of ingenious twists in the plot.

Are You Positive? features a trial that has, unfortunately, some real-life precedents: an HIV-positive man on trial for transmitting the virus to a sexual partner. As in the earlier book, the real-life models of some protagonists are recognizable, including by their initials. The evidence is unfolded at digestible pace: the lack of validity of “HIV” tests, the racial bias of the tests, the particular likelihood that TB patients and pregnant women will test “HIV-positive”. The recommendation that everyone be tested is mentioned, and the gruesome story of the orphans used as guinea pigs in clinical trials. The Padian study revealing lack of sexual transmission is dissected expertly. Gallo’s scientific failings are described accurately, as well as his self-incriminating testimony in the Parenzee trial in Adelaide (Australia). The role of conflicts of interest in the HIV/AIDS industry is brought out. An Appendix has a recommended “Informed Consent” form that people should require their doctors to sign if they are being asked to take an HIV test.

The story is told very accurately indeed in this novel. Because I already knew that every detail is correct, I found it emotionally difficult reading–I know of a dozen people languishing in jail for the crime of making love while testing “positive” for a supposedly active infection that the tests cannot actually establish, and there are surely many more in jail of whom I am not aware. HIV/AIDS-naïve readers, however, may not experience that emotional burden as they are led slowly to doubt what the conventional wisdom insists on.

My respect for these books and their author was only increased when, toward the end, I found cited one of my favorite epigrams, one I had used myself for years as the motto of a newsletter I once edited:

All that is necessary for the triumph of evil is for good men to do nothing

Both these books are paperbacks published via automated “on demand” printing. Their material quality is comparable with such productions from large publishers, but in their lack of typographical errors they are far superior to most contemporary works, including in hard covers from long-established and respected presses.

Rethinkers ought to consider giving these books to their friends and acquaintances who scoff at the possibility that the mainstream could be wrong about HIV/AIDS. Leading HIV/AIDS-naïve people through salient details of the evidence in measured and linear succession is likely to make it easier for them to begin to shake off unthinking acceptance of the conventional wisdom than trying to argue all the scientific issues in concentrated form. Wrongful Death cites hundreds of supporting published sources; Are You Positive? relegates them to the website. In both cases, you can assure those to whom you give these books that the cited evidence is solidly supported in the mainstream literature and that the cited sources represent fairly the totality of what has been published and what is known.

DEATH, ANTIRETROVIRAL DRUGS, and COGNITIVE DISSONANCE

No sooner had I remarked on cognitive dissonance (HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE, 29 April 2008 ) than a truly hair-raising instance of it turns up: the increasing rate of deaths caused by antiretroviral drugs is said to require clinical trials in which these drugs would be tried out on even healthier people.

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Most “AIDS” deaths now are from liver failure, cardiovascular problems, and the like, which are clearly “side” effects of the antiretroviral drugs. By refusing to acknowledge this, however, a recent article interprets the data as calling for administering these drugs to even more people, people whose immune systems are even healthier by the official criterion of CD4 counts in the blood. Under the current guidelines, treatment is recommended for asymptomatic HIV-positive people who have never had an AIDS illness at CD4 counts <200, and it is said to be optional between 200 and 350. Now, it is suggested, treatment should perhaps be recommended at counts even higher than 350:

“Reductions in AIDS-related morbidity and mortality following the advent of combination antiretroviral therapy have coincided with relative increases in chronic non-AIDS end-organ diseases among HIV+ patients….
Higher CD4+ counts on antiretroviral therapy are associated with lower rates of non-AIDS diseases and AIDS. These findings … motivate randomized studies to evaluate the effects of antiretroviral therapy on a broad set of clinical outcomes at CD4+ counts greater than 350 cells/µl.” (emphasis added; Baker et al., CD4+ count and risk of non-AIDS diseases following initial treatment for HIV infection, AIDS 22: 841)

That recommendation is based on the belief that antiretroviral drugs increase CD4 counts, and that higher CD4 counts are not only somehow associated with better health but actually cause better health and prognosis. That belief is not justified by much and long-accumulated data, however. It’s been known at least since the Concorde results published in 1994 that CD4 counts (in the blood) do not correlate with better clinical outcomes, and the large Antiretroviral Collaboration published in 2006 reported that HAART increased rather than decreased the incidence of adverse events (sources cited at p. 169 in The Origin, Persistence and Failings of HIV/AIDS Theory). In between there have been a range of articles pointing the same way, for example the finding that viral load and CD4 counts are not correlated:

“Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection” (Rodriguez et al., JAMA, 296 [2006] 1498-1506).

Note that the decline of CD4 counts in HIV-positive people remains to be explained and is not owing to the amount of purported virus measured supposedly by viral load.

Yet Baker et al. in their 2008 publication cite a 1997 paper for the beneficial effect of HAART in restoring CD4 counts, while neglecting to mention “immune restoration syndrome”, described already in 1999: the phenomenon in which supposedly restored immune-system function leads to death rather than health; and Baker et al. cite a 1998 paper reporting declining mortality, very few years after HAART was introduced, while ignoring the Antiretroviral Collaboration published in 2006 that found increased mortality.

Correctly cited are no fewer than 10 independent studies, published between 2002 and 2007, that found increased incidence of and death from liver, cardiovascular, and renal diseases, and from some cancers, among HIV-positive people on antiretroviral treatment. In their own study, remarkably, Baker et al. want to ascribe this to “prolonged survival” achieved by antiretroviral treatment. Yet the median ages of their patients who suffered or died from these non-AIDS illnesses was between 40 and 44, ages at which one does not normally expect a noticeable rate of death from cancer, or from liver or heart “end-organ” failure. Those conditions are typical effects of drugs.

Not only does the selective citation of data and the manner of interpretation adopted by Baker et al. allow much room for questions to be raised, so does the very manner in which they report the data. Here is their summary (their Table 1; “FIRST” is an acronym for the Flexible Initial Retrovirus Suppressive Therapies trial):

Please look at the numbers carefully. 188 total deaths are reported, of which 89 are from AIDS and 27 from non-AIDS “events”. “AIDS” and “non-AIDS”, one might imagine, are mutually exclusive categories that together cover all possibilities; yet 188 minus 89 minus 27 leaves 72 deaths unaccounted for.

Only several paragraphs below the table are these referred to: “16 were a result of sepsis/shock, 17 from respiratory failure or pneumonia, 17 from other cardiovascular causes (arrhythmia, heart failure, pulmonary embolus, or aneurysm), and 20 were due to unknown causes”.

How are these 17 cardiovascular-caused deaths different from the 5 reported in the Table as “non-AIDS cardiovascular”, since apparently they are not “AIDS”?

Why were not all those 72 deaths acknowledged as “non-AIDS”?

What possible reason is there not to regard these deaths as plausibly occasioned by the antiretroviral drugs?

Furthermore, what is one to say about a study in which 20 deaths — 20 out of 188, a little over 15% — are attributed to unknown causes? Who was in charge here? How were the patients being monitored? Who signed the death certificates? Why were no autopsies performed in cases of doubt about the cause of death? In a study specifically aimed at elucidating ways of decreasing mortality, what possible excuse is there for such lapses? (And, not by the way, what does this say about the quality of the editorial review and refereeing practices of this journal?)

Enough of rhetorical questions: There were actually 99 non-AIDS deaths and 89 AIDS deaths. All the causes of the non-AIDS deaths are conditions typically associated with “side” effects of drugs. Since the median age of the patients was about 40, it is more than plausible that they were caused by the antiretroviral drugs. Indeed, the latest version of the official Treatment Guidelines states (at p. 13):

“In the era of combination antiretroviral therapy, several large observational studies have indicated that the risk of several non-AIDS-defining conditions, including cardiovascular diseases, liver-related events, renal disease, and certain non-AIDS malignancies … is greater than the risk for AIDS in persons with CD4 T-cell counts >200 cells/mm3; the risk for these events increases progressively as the CD4 T-cell count decreases from 350 to 200 cells/mm3.”

When there are more deaths from scenario A than from scenario B, one might prefer the latter. In other words, better NOT to use antiretroviral treatment, especially with people who initially present with no symptoms of illness and who are treated only because of laboratory tests (“HIV” and CD4) of doubtful validity and significance.

But even accepting the article’s basic premises, note that there is mention of only a correlation between CD4 counts and risk. Anyone should feel free to interpret all this differently, namely: People with higher CD4 counts (in the blood) are better prepared to stave off physiological insults than those with lower counts, and they are therefore better able to resist the toxic effects of antiretroviral drugs. Apparently, the higher one’s CD4 count, the longer one is likely to survive HAART. Recall Julianne Sacher’s explanation of why CD4 counts in the blood vary dramatically from time to time: these cells move to those parts of the body that are under attack (AIDS AS INTESTINAL DYSBIOSIS, 23 February 2008; ALTERNATIVE TREATMENTS FOR AIDS, 25 February 2008).

Baker et al., however, choose to sum up their findings thus:
“Serious non-AIDS diseases, such as liver, cardiovascular, renal, and non-AIDS cancers, have contributed significantly to morbidity and mortality among HIV-infected patients because of the introduction of potent combination ART. It is unclear to what extent this is due to chronic immunosuppression, complications of ART, coinfection, or other established risk factors . . . .
we have established an association between latest CD4+ levels and risk for end-organ diseases not attributable to AIDS following initiation of ART. Further research is needed to establish whether HIV-related immune depletion truly leads to more frequent non-AIDS diseases, and to examine the underlying mechanisms.”

In my view, it is implausible to the point of perversity to suggest “chronic immunosuppression, coinfection, or other established risk factors” as possible reasons for the increased mortality in the same breath as “complications of ART”, given that all the death events are from occurrences well known to typify iatrogenic events; they are typical “side” effects of drugs.

It also seems to me highly irresponsible to suggest “further research” that involves exposing yet more and healthier people to drugs whose toxicity is beyond doubt.

RACIAL DISPARITIES IN TESTING “HIV-positive”: IS THERE A NON-RACIST EXPLANATION?

Whenever people in the United States have been tested for “HIV”, members of the officially recognized racial groups have yielded different results: blacks always test “HIV-positive” more often than others, Asians always test “HIV-positive” less often than others. Whites test “HIV-positive” significantly more often than Asians, Native Americans somewhat more often than whites, and Hispanics significantly more often than Native Americans.

The same racial bias in “HIV” tests is found in other parts of the world: within South Africa (pp. 75-6 in The Origin, Persistence and Failings of HIV/AIDS Theory); between sub-Saharan Africa and northern Africa; within the Caribbean; in Europe (HIV: THE VIRUS THAT DISCRIMINATES BY RACE, 11 April 2008; HIV: A RACE-DISCRIMINATING SEXUALLY TRANSMITTED VIRUS!, 16 April 2008; DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

A comprehensive recent review acknowledges the racial bias in testing “HIV-positive”:
“racial and ethnic minorities, especially African Americans and Hispanics, are disproportionately affected….
in Europe … many infections today are found among immigrants from sub-Saharan Africa” (Cohen et al., Journal of Clinical Investigation 118 [2008] 1244-54).

The racial disparities in testing “HIV-positive” are as firmly accepted in mainstream discourse as any aspect of HIV/AIDS is.

WHY? Why are “HIV” tests racially biased?

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For reasons that need no reiterating, deep and delicate sensitivities are aroused by any discussion of human differences associated genetically with the commonly used racial designations. One should therefore bear in mind that race is a matter of biology, not at all the same thing as perpetrating racism, which is a matter of social practices and public policy. The eminent anthropologist Ruth Benedict had wise things to say on this score (Race and Racism, first published 1942; page references from 1983 edition, Routledge & Kegan Paul):
—“a student may have at his tongue’s end a hundred racial differences and still be no racist” (p. vii)
—“Race is not ‘the modern superstition,’ as some amateur egalitarians have said. It is a fact. . . . Race . . . is not the modern superstition. But racism is.” (pp. 96, 97)

Benedict makes clear the distinction between race and culture. Race is a biological matter having to do with phenotypes, genotypes, DNA, physiology, colors of eye and hair and skin, and so on. Culture is a matter of learned behavior, and culture and behavior are not determined by race; innumerable cultures have maintained their distinguishing characteristics while the racial composition of the people expressing those cultures changed; and no race has always expressed some unique culture of its own everywhere.

“Race” is a very crude biological classification. There are only half-a-dozen or so human groups in the typical list of “races”, and there is enormous genetic variation among members of any one of these groups. Yet the classification has its uses, particularly perhaps in medicine, in view of significant statistical associations of race with predisposition to such conditions as Tay-Sachs disease or sickle-cell anemia.

But it is rather few predispositions that are significantly linked to this crude classification into half-a-dozen racial groups. That’s what makes the racial disparities in testing HIV-positive so extraordinarily difficult to explain on the basis of HIV/AIDS theory. Testing “HIV-positive” is unquestionably linked to biological race. HIV/AIDS theory ascribes testing “HIV-positive” to behavior. Thus HIV/AIDS theory appears to require that sexual and drug-abusing behavior be determined by biological race to an extent that is seen with rather few other characteristics and that has certainly not been found with any other form of behavior.

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If HIV is an infection transmitted predominantly via sex, then racial disparities in its distribution have to be explained in terms of racial disparities in sexual behavior. That is contrary to the evidence, and it is contrary to what anthropology and biology and psychology and sociology know. Is there any way in which racial disparities as to HIV could be explained in non-racist terms?

One would have to postulate that there are racially linked genes that influence how a person reacts when exposed to the virus. Perhaps people with certain genetic traits are more likely to be infected upon exposure? In that case, one would not have to ascribe racial disparities in rates of actual infection to differential rates of exposure, that is, differences in sexual behavior.

Much research has aimed to identify genetic factors that make for resistance to “HIV infection” or resistance to progression to AIDS after “infection” (or seroconversion), by studying so-called “long-term non-progressors” or “elite controllers” or individuals persistently exposed to HIV without seroconverting. These searches have remained unsuccessful. It has become something of a shibboleth that genetic variants of CCR5, a “co-receptor” of HIV, provide resistance, but this does not begin to accommodate the facts as to racial disparities: the pertinent allele is found “at high frequency in European Caucasians (5%-14%, with north-south and east-west clines) but is absent among African, Native American, and East Asian populations”; but non-CCR5-protected Asians resist “HIV” even more strongly than supposedly-CCR5-protected Caucasians, and Africans are affected by “HIV” far more than are Native Americans. Moreover, the CCR5 allele in question appears to have been the subject of neutral evolution over thousands of years and certainly was not selected for under the pressure of supposedly fatal infection by “HIV” (Sabeti et al., PLoS Biology 3 [(#11, 2005] e378.) http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371%2Fjournal.pbio.0030378

The facts as to a putative resistance to infection also speak quite stubbornly against such a phenomenon. The probabilities of apparent transmission are the same for blacks, whites, and south-east Asians, always on the order of 1 per 1000 acts of unprotected intercourse (relatively more for male-to-female and less for female-to-male), according to (at least) three published reports from Africa, one each from Haiti and Thailand, and nine from the United States (individual sources cited at p. 44 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory).

Since the apparent probability of transmitting “HIV-positive” displays this remarkably reproducible figure of about 1 per 1000, differences in prevalence of the “HIV-positive” condition can only be ascribed—under HIV/AIDS theory—to differences in frequency of exposure or type of sexual behavior.

There is no way around it. To accept HIV/AIDS theory means to accept that there are characteristic differences in sexual behavior between Asians, Caucasians, Native Americans, Hispanics, and blacks; and, among Hispanics in the United States, characteristic differences in sexual activity between the East and West coasts, differences that happen also to run parallel to differences in racial ancestry. That requires acceptance of a radically extreme version of sociobiology, namely, that sexual behavior is determined genetically and not culturally. Such acceptance also constitutes what Ruth Benedict correctly described as racism and as contrary to fact.

“HIV” IN PRISONS: REGULAR AS CLOCKWORK

A clear disproof of HIV/AIDS theory is the fact that the demographics of “HIV-positive” are constant: the geographic distribution has not changed in two decades, neither has the rate at which people test positive; and the racial disparities have remained the same. The numbers given in my book continue to be replicated by other and by later reports, see for example REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”, 1 April 2008. The latest report on “HIV” in prisons once again replicates salient trends:

The overall rate of “HIV-positive” in prisons, 2004-2006, was 1.7-1.8%; most of the cited sources in my book reported 2-3%. More strikingly, the geographic distribution is once again the same: Northeast (3.9%) > South (2.2%) > Midwest (0.9%) and West (0.7%).

The same geographic distribution is seen among prisoners as among military cohorts including applicants, new mothers, blood donors, members of the Job Corps, and the totality of public testing sites. The geographic distribution of “HIV-positive”, in other words, is not a function of social status or circumstances, and it is not a function of time, having remained without significant change for more than twenty years.

Moreover, the geographic distribution can be calculated simply from the racial disparities in testing “HIV-positive” and the racial composition of the population in each region (DECONSTRUCTING HIV/AIDS in “SUB-SAHARAN AFRICA” and “THE CARIBBEAN”, 21 April 2008).

“HIV-positive” is not the mark of an infectious agent.

HIV/AIDS ILLUSTRATES COGNITIVE DISSONANCE

Oh that one would hear me! … and that mine adversary had written a book
King James Bible, JOB 31:35

As a target of debunking, a review may serve as well as a book, especially when it happens to be a review of what’s [not!] known about HIV/AIDS: “The spread, treatment, and prevention of HIV-1: evolution of a global pandemic”, by Myron S. Cohen, Nick Hellmann, Jay A. Levy, Kevin DeCock, and Joep Lange, Journal of Clinical Investigation, 118 [2008] 1244-54; doi:10.1172/JCI34706. The authors are heavyweight white-coated HIV/AIDS gurus, at least two of whom (Levy, DeCock) have been in this business from the beginning. The review is a textbook case of cognitive dissonance or, using Thomas Kuhn’s term, incommensurability (1).

Cognitive dissonance is the inability to “see”, or to comprehend the implications of, evidence that—objectively speaking—disproves a belief. Popular parlance might describe it as a state of denial. In Festinger’s classic study (2), when the predicted end of the world did not come on the calculated date, the believers concluded only that they had gotten something in the calculations a bit wrong, and their basic belief hardened rather than weakened.

“Incommensurability” signifies that researchers get so vested in the prevailing paradigm (i.e., dogma) that they cannot understand—quite literally cannot understand—how data could be interpreted in any other fashion than the one dictated by their belief.

Imre Lakatos (3) identified a strategy researchers use quite routinely to preserve belief in the face of contradictory evidence: they invent ad hoc explanations for each new piece of data that their theory cannot accommodate. They do not modify at all the basic belief (the “core theory”); rather, they attach to it ad hoc extensions that are not genuine corollaries because they are not inherently demanded by the theory, and they are not necessarily consistent in any natural way with other such ad hoc extensions of the theory.

This aspect of science is not part of the conventional wisdom about “science”; the popular myth, oversimplified and reverential, holds science to be trustworthy under all circumstances (4, 5). But illustrations of the fallibility of science abound, and HIV/AIDS dogma offers some cogent examples of cognitive dissonance, for example:

— The prediction that the AIDS outbreaks in major American cities would be followed by a spread into the general population was almost immediately falsified; yet the belief that HIV is sexually transmitted hardened rather than weakened.

— The prediction that a vaccine would be available within a couple of years after 1984 has been falsified over and again, despite the deployment of every conceivable strategy for design of such a vaccine, not to speak of untold millions of dollars expended. These failures have brought only increasingly strident calls to continue the attempts.

— The finding that the observed apparent rate of sexual transmission is far too low to explain the observed distribution of “HIV-positive” people was met by the ad hoc postulate that there must be some higher rate of infectivity during short periods; and this unobservable and unobserved infectiousness is nowadays dogma without the benefit of proof.

The cited review by Cohen et al. of the state of the art of HIV/AIDS offers further illustrations of accepting as fact, and disseminating as fact, things that are plainly not true, or that are unproven or unprovable, or that border on the absurd. As well, interpretations are invoked or implied that in other contexts would be immediately recognized as unwarranted, and racist to boot.

Simply wrong:

“[M]ale circumcision provides substantial protection from sexually transmitted diseases, including HIV-1”
Four references are given, but left unmentioned is the study by the Centers for Disease Control and Prevention (6), which found no such effect.
Even were such an effect to be suggested by correlations (which are the only available evidence), one might question a causal interpretation for its extreme implausibility with respect to “HIV-1”: how could circumcision protect males from an agent whose apparent transmission from female to male is already significantly lower than the apparent transmission from male to female, which itself is only about 1 in 1000? And given those almost immeasurably small apparent rates of transmission, how massive a set of trials would be needed to gather potentially convincing evidence?
As to circumcision protecting against known STDs, there is controversy extending over centuries and still not resolved to the satisfaction of all researchers, see http://www.circumcision.org/. For example, Professor Andrew Grulich (National Centre in HIV Epidemiology and Clinical Research [Australia]) reported recently at the Australasian Sexual Health Conference (Gold Coast, 11 October 2007) that there was no association between infection and circumcision status for any disease apart from syphilis (Thaindian News, 14 November).

Hardened belief in face of contrary facts:

“28 years after AIDS was first recognized…, HIV-1 requires continued global focus and investment”
Required, presumably, only because researchers want the money; for in the very same paragraph, Cohen et al. acknowledge that “global HIV-1 prevalence seems to have been stable since around the turn of the 20th century; and HIV-1 incidence peaked worldwide in the late 1990s and has been declining ever since”.

“Perhaps one of the most surprising aspects of the HIV/AIDS pandemic is the unequal spread of HIV-1”
Exactly; “surprising” because no infectious agent behaves like that.
On the one hand, “HIV-1 does not respect social status or borders”—because no sexually transmitted agent does—yet on the other hand, “racial and ethnic minorities, especially African Americans and Hispanics, are disproportionately affected… in Europe … many infections today are found among immigrants from sub-Saharan Africa”. The obvious contradiction between “no borders” and “racially discriminatory” can only be resolved by recognizing that HIV is not sexually transmitted; but those hewing to the dogma are incapable of that recognition, as Festinger, Kuhn, and others have pointed out.

“Africa has witnessed the full devastation of the HIV/AIDS pandemic”
but the population there has continued to grow at an annual rate of a few percent!

Swallowing improbabilities:

“DNA sequences of viruses in distinct clades can differ by 15%-20%”
and yet all of them are supposed to do about the same thing, with only minor differences in efficiency of transmission and “pathogenic potential”.
But in other contexts we’re told that human and chimp genomes differ by less than 1%, which suffices to produce quite major differences in the products of those genes.

“In Eastern Europe … brisk and severe epidemics emerged among injecting drug users in the late 1990s”
Grant—for the moment—that HIV can be transmitted via infected needles: how to conceive “brisk and severe epidemics” from shared needles? Try to picture the orgies of needle-sharing that would be required, particularly when two decades of experience have revealed that catching “HIV-positive” from needle punctures is even less probable than the 1 in 1000 chance via unprotected intercourse.

How HIV is transmitted in different parts of the world:

Since this figure sports precise percentages, the casual observer might be tempted to regard this as scientifically established fact, instead of pausing to recognize how absurd it is on its face. Marital sex responsible for half of all infections in the most affected area, and for a quarter of them in Asia—but not at all in Eastern Europe? Casual sex more significant in Eastern Europe than transmission among men who have sex with men, who remain in the United States the group most regarded as at risk?! Mother-to-child transmission (MTCT) virtually unknown outside Africa, including in Asia where “marital sex” represents a quarter of all transmission?? Doesn’t marital sex in Asia ever lead to pregnancy?!? Medical injections, too, virtually unknown outside Africa; and in Africa allowed just a few percent, ignoring the numerous publications by Gisselquist, Potterat et al. that indict such injections as a more plausible source of the “pandemic” than sexual intercourse?!?! Sex workers a substantial risk in Asia and Latin America, but far less dangerous than marital sex in Africa, and no risk at all in Eastern Europe?!?!?
To believe all this, one would have to also believe that these various regions of the globe are characterized by cultures and lifestyles so different as to bespeak the presence of altogether different species of Homo.
The text of the review article notes that “the US epidemic remains a paradigm of HIV/AIDS in the developed world”, indicates that sex among males is the greatest source of infections there, and suggests something similar for Western Europe. Those are the regions for which the data are most copious and reliable; and moreover North America is the region where HIV/AIDS originated, the veritable “mother of all HIV/AIDS regions”; so why are Western Europe and North America absent from the figure, whose source is “Bringing HIV prevention to scale: an urgent global priority”?

Subterranean racism:

“even in settings of generalized epidemics [i.e., self-sustaining in the population], the risk of infection with HIV-1 is … increased in persons with higher rates of partner change or who acquire classical … STDs … [or] who experience other significant exposure(s) to HIV-1, such as injection drug use”
— those people who also happen to be endowed with black skin, in other words, because all our data has shown for a couple of decades that they, everywhere in the world, are the most likely to test “HIV-positive”: “In the US, racial and ethnic minorities, especially African Americans and Hispanics… in Europe … many infections today are found among immigrants from sub-Saharan Africa”.

Note how the term “minorities” is deployed as a euphemism in mainstream discourse about HIV/AIDS (and in many other contexts too). In the United States, Asians constitute a much smaller numerical minority, and Native Americans an even smaller minority again, than either blacks or Hispanics. But Asians are significantly less affected by “HIV” than are white Americans, and Native Americans are affected not much more than Caucasians and significantly less than Hispanics, let alone blacks. “Minorities” serves as a euphemism for both “liable to reprehensible behavior” and “black”.

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This review article constitutes a goldmine of additional opportunities to debunk HIV/AIDS theory. It is replete with unproven assertions, for instance about “acute viral syndrome”, and contains the occasional nugget of acknowledgment that the most fundamental, central, matter of all remains as mysterious as when it was first declared that HIV destroys the immune system:

“To date, the destructive properties of HIV-1
have not been completely unraveled”.

If one omits the misleading euphemistic weasel-word, “completely”, this statement is demonstrably true. None of the many suggested mechanisms have stood the test of reality. No plausible mechanism for the destruction of the immune system by HIV has been discovered in a quarter century, following more than $100 billion spent on research.

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References:
(1) Thomas S. Kuhn, The Structure of Scientific Revolutions, University of Chicago Press (1970, 2nd ed., enlarged; 1st ed. 1962)
(2) Leon Festinger, Henry Riecken, & Stanley Schachter, When Prophecy Fails: A Social and Psychological Study of A Modern Group that Predicted the Destruction of the World, University of Minnesota Press (1956)
(3) Imre Lakatos, “History of science and its rational reconstruction”, pp. 1-40 in Method and Appraisal in the Physical Sciences, ed. Colin Howson, Cambridge University Press (1976)
(4) Henry H. Bauer, Fatal Attractions: The Troubles with Science, Paraview Press (2001)
(5) Henry H. Bauer, Scientific Literacy and the Myth of the Scientific Method, University of Illinois Press (1992)
(6) Millett GA et al., “Circumcision status and HIV infection among Black and Latino men who have sex with men in 3 US cities”, JAIDS 46 (2007) 643-50