Nobel Prize Citation for “HIV” “Discovery”: Errors and Deficiencies
Posted by Henry Bauer on 2008/10/16
The initial appearance of AIDS is said to have been in “clusters of previously healthy young men”, repeating mindlessly a worn, faulty shibboleth. Michelle Cochrane (When AIDS Began: San Francisco and the Making of an Epidemic, 2004), however, looked at the original medical records and found that they were anything but “previously healthy”, and “young” would apply only if that is taken to mean people in the middle to upper 30s (The Origin, Persistence and Failings of HIV/AIDS Theory, p. 187 ff.).
It is more subtly misleading, but misleading nonetheless, to say that they “suffered from different life threatening medical conditions”. A crucial clue to what AIDS really was in the early 1980s is the fact that the original victims displayed predominantly two types of condition: Kaposi’s sarcoma (KS), a disorder of blood vessels that was almost certainly the direct result of excessive inhalation of nitrites, and fungal infections — chiefly Pneumocystis carinii pneumonia (PCP) and candidiasis — that followed excessive indulgence in practices that destroy the intestinal microflora which normally keep those endemic fungi in check [see Tony Lance, “Gay-Related Intestinal Dysbiosis”, in “What really caused AIDS: Slicing through the Gordian Knot”, 20 February 2008]. Those two types of condition accounted for more than 80% of the 16,000 AIDS cases recorded through 1985; that percentage decreased gradually only after “HIV-positive” rather than clinical condition became the criterion for an AIDS diagnosis.
The assertion, “A huge epidemiological survey initiated by CDC in 1982 concluded that the AIDS syndrome had spread globally”, lacks a sorely needed specific reference.
The CDC Report for 8 July 1982 cites 452 cases, 441 from 23 states in the USA and only 11 from other (unnamed) countries. Reports for 1983 and later refer specifically only to the United States. The Morbidity & Mortality Weekly Report of 24 September 1982 mentions 597 cases within the USA and an additional 41 cases from 10 foreign countries. That hardly seems like the outcome of a “huge epidemiological survey” that discovered a global epidemic.
“A subset of the population at particular risk for this syndrome appeared to be homosexual males and intravenous drug users” is also subtly misleading about a condition that seemed and seems to be virtually restricted to those groups in most parts of the world.
“The immunodeficiency was associated with rapid elimination of CD4+ T cells” cites 71: Gottlieb MS, Schroff R, Schanker HM, and Saxon A. Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men: evidence of a new acquired cellular immunodeficiency. N Engl J Med. 1981;305:1425-31, which does “associate” — correlate — AIDS with low CD4+ counts, but doesn’t and could not speak to “rapid elimination” (as well as being wrong about the “previously healthy”, see above). Gottlieb et al., moreover, reported in detail on only 4 cases, hardly a basis for any sweeping generalization; and the association they thought most pronounced was with cytomegalovirus.
“The clinical AIDS spectrum was defined as repeated opportunistic infections . . . occurring in previously healthy adults with no history of inherited disorders” follows a sentence mentioning haemophiliacs among the risk groups; yet haemophiliacs do have an inherited disorder.
An interesting sentence is [emphases added] “Malignancies associated with AIDS included an aggressive type of Kaposi’s sarcoma caused by human Herpes virus 8, EBV-associated lymphoma, HPV-induced cervical cancer, and Hodgkin’s disease (75)”. Thus it is clearly acknowledged that at least 3 of the 4 malignancies are caused by something other than HIV; and moreover the citation is wrong: (75) is “Rozenbaum W. Multiple opportunistic infections in a male homosexual in France. Lancet. 1982; 6;1(8271):572-3”, a letter of 5 paragraphs in which none of those malignancies is mentioned.
“The disorder also manifested as slim disease due to chronic incurable diarrhoea, particularly in Africa”. So: is “chronic incurable diarrhoea” an opportunistic infection owing to immunedeficiency, or perhaps a malignancy?
“Epidemiological studies had already been [sic] established that AIDS was transmitted sexually, via placenta to foetuses and via transfusion by plasma and coagulation products (76)”; 76 is: Francis DP, Curran JW, Essex M. Epidemic acquired immune deficiency syndrome: epidemiologic evidence for a transmissible agent. J Natl Cancer Inst. 1983;71(1):1-4.
That article does much less than “establish” those things (in fact, the piece is labeled a Guest Editorial, hardly the sort of thing one cites as “establishing” anything). That “the syndrome has appeared almost simultaneously in socially disparate and distinct population groups who share only their predilection for other infectious diseases” merely suggests a connection with sexually transmitted diseases, while avoiding the issue of outbreaks distributed in widely separated geographic locations. That “80% . . . [of AIDS victims were] between 25 and 44”, on the other hand, hardly points to an infectious agent, since those are typically more dangerous to the very young and the very old. The remark [emphasis added] that “this putative agent must circulate in the blood” again does much less than even claim to “establish” an infectious cause. Moreover, Francis et al. acknowledge that any unifying hypothesis encounters the dilemma that KS occurs almost exclusively in only one of the risk groups. Hindsight reveals that this editorial was also wrong on two rather important counts: that PCP is a fungal infection, not a parasitic one, and that the supposed latent period is on the order of 10-15 years (the Nobel Committee’s estimate) rather than ≥12 months.
“A number of pieces of evidence pointed towards a retroviral origin for the acquired immune deficiency; the clusters of patients affected, the transmission via filtered blood products and the establishment of loss of CD4 T helper lymphocytes” is an extraordinary statement; there was no precedent for a retrovirus killing off CD4 cells, so how could this “point towards” such an interpretation? Furthermore, transmission by filtered blood would indicate a virus, but not necessarily a retrovirus. That clusters of people were affected doesn’t even indict an infectious agent, it could be an environmental factor, like — say — the gastric cancers in Chinese and other locations where nitrites or nitrosamines are for some reason present in exceptionally high amounts (e.g., You et al., Cancer Epidemiology, Biomarkers & Prevention 5  47-52).
The “discovery” of the “retrovirus” is described in considerable detail, the salient step being the first one: “Virus production was detected by reverse transcriptase (RT) enzyme activity in supernatants from cultured and activated lymphocytes obtained from a lymph node from a patient with lymphadenopathy”; “They cultured purified lymphocytes from such patients in vitro in the presence of the phytohaemagglutinin (PHA)-mitogen, interleukin-2 (IL-2) and anti-interferon-a in order to allow T cell proliferation” — in other words, as several Rethinkers have pointed out, the “virus” was created in a witch’s brew designed to stimulate proliferation of the very cells supposedly killed by the virus; and the presence of a retrovirus was inferred from the fact of reverse transcriptase activity — and, later, it turned out that such activity is routinely present as part of normal cell function. There was no isolation of virus particles from a supposedly infected individual.
And so on. Rethinkers will relish such statements as “In 1985 the nucleotide sequence of the full AIDS virus genome was established”, since this was done by indirect inference without ever having access to a genuine virion. It may turn out to be unwittingly prescient, though, that “The retrovirus family consists of the Oncovirus (including HTLV-I & -II), Lentivirus (including HIV-1 &-2) and Spumavirus also called foamy virus and the so far considered non-pathogenic, Endogenous retrovirus”, since “HIV” could well belong to the Endogenous and non-pathogenic class.
The origin and spread of “HIV” in Africa are illustrated nicely by a Figure showing transmission routes out of Cameroon (thick brown lines with arrows, arrowheads enhanced for easier viewing):
However, it is not explained why the virus has remained largely in southern Africa rather than in the other places to which it headed and which are closer to its origin, though that fact is properly illustrated in another Figure:
Note, by the way, that the USA is relatively little “infected” even though this was where AIDS first appeared; and that Eastern Europe and Russia are significantly more infected even though the epidemic there is said to be carried largely by injecting drug users! [“HIV/AIDS illustrates cognitive dissonance”, 29 April 2008]. This Figure also displays the extraordinary ability of “HIV” to quarantine itself at regional boundaries. One might also quibble about the choice of a category of “1.0 – ≤5.0 %”, since this gives the Russian Federation, at an estimated 1.1%, a deeper color and more prominent presence than almost any other region outside Africa, the others being Papua at 1.8%, Thailand at 1.4%, and thereby understates how quarantined middle and southern Africa at ≥5% are from the rest of the world at ≤2%.
The detailed description of how HIV works is rather at odds with the several publications which confess that this remains a mystery, for example, “The pathogenic and physiologic processes leading to AIDS remain a conundrum” (Grossman et al., Nature Medicine 12  289-95); and the Nobel description is itself a shade mystifying, for example, “Immune activation and inflammation supplies additional activated CD4+ T cells, which both sustain infection and elicit an immunosuppressive response that blunts host defences. Although increasing numbers of cytotoxic T lymphocytes (CTLs) partially control infection they do not prevent, in the absence of therapy, the slow and continued depletion of CD4+ T cells that is responsible for the occurrence of the immune deficiency that eventually leads to AIDS” [emphases added]. This is a fascinating double-barreled action during the postulated latent period of about 10 years during which “viral load” is very low; with the explanatory barrels pointing in opposite directions, that seems rather hazardous to one’s (mental) health. There are similarly puzzling explanations of “host defence” and its sophisticated evasion by “HIV”. None of these explanations are labeled speculative, as they should properly be.
The Nobel Committee’s erratic citation practices are illustrated also by “The discovery of HIV allowed for a rapid dissection of the viral replication cycle (Fig 13) (129)”, which led me to think that reference 129 would recount that “rapid dissection”. Instead, it is an article in press (as of 15 October, “Please cite this article in press as: Greene, W.C., et al., Novel targets for HIV therapy. Antiviral Res , doi:10.1016/j.antiviral.2008.08.003”); and it is a review of the search for “Novel targets for HIV therapy”, brief summaries of talks presented at the 21st International Conference on Antiviral Research held in April 2008 in Montreal; such a search certainly being needed in view of “the emergence of drug resistance and various adverse effects associated with long-term use of antiretroviral therapy”. That review has a useful table of antiretroviral drugs and their date of approval. The earliest, AZT (zidovudine, ZDV, Retrovir), approved in 1987, owed nothing to an understanding of the viral replication cycle; the next two, ddI and ddC in 1991 and 1992, were designed — like other nucleoside/nucleotide reverse transcriptase inhibitors (NNRTIs) — to work in the same manner as AZT. It’s not at all clear how the purported specific understanding of the viral replication cycle is supposed to have served to develop those drugs; but implying that certainly lends an impressive flourish to this just-so story of science at work.
That just-so story continues, “It rapidly became clear that the ability of HIV-1 to generate drug-resistant mutants meant that therapy would require a combination of agents affecting different proteins involved in viral replication (130, 131). . . . subsequent development was focused on the protease enzyme” [emphasis added]. Once again, “rapidly” makes the “science” appear more impressive than it was in practice, for it was a decade between AZT and the first protease inhibitors. The spurious claim is repeated, that “combination therapy . . . has dramatically increased the life expectancy of AIDS patients in developed countries”: as the death statistics plainly show, there has been no dramatic increase in the median age at which people die of “HIV disease” — “HAART saves lives — but doesn’t prolong them!?”, 17 September 2008; ”Virological response after starting HAART improved over calendar years, but such improvement has not translated into a decrease in mortality” (Antiretroviral Therapy [ART] Cohort Collaboration, Lancet 368  451–58) — in other words, HAART decreases “viral load” but doesn’t prolong lives, so “HIV” is irrelevant to clinical progression.
In this connection, the Nobel citation is subtly misleading when it says, “successful antiretroviral therapy results in life expectancies for persons with HIV infection now reaching similar levels to those of uninfected people” — of course, “successful” therapy does so, but there is apparently a great deal of UNsuccessful therapy: the majority of adverse events under HAART are “non-AIDS” events, i.e. iatrogenic, the “side” effects of therapy, namely, liver or kidney or heart failure (Treatment Guidelines, 29 January 2008, p. 13) . So it’s rather horrifying that “Currently, 3 million people are being treated with anti-retroviral drugs”; if the USA data from 1996 to 2004 are any guide, then these 3 million will die at an average age in the middle forties.
The Nobel citation also treats as proven fact the notion that the CCR5d32 deletion is protective, though that notion proved to be an illusion — “Racial disparities in testing “HIV-positive”: Is there a non-racist explanation?”, 4 May 2008.
Finally, the citation skates rather too lightly over the failure to generate a vaccine: “attempts to develop a protective vaccine
have been severely compromised by our incomplete understanding of HIV-1 protective immunity” should more accurately read, “researchers haven’t a clue as to what might provide protective immunity”.
The Conclusions are no better than the main text. “The discovery . . . made it possible to perform molecular cloning of HIV-1” — without ever having isolated an authentic virion of HIV! The triumphalism is simply not warranted by the facts: “unravelling of important details of its replication cycle and how the virus interacts with its host” — which is still not understood. Diagnostic tools followed “quickly . . . which has limited the spread of the pandemic” — not according to the continuing alarms emanating from UNAIDS and WHO about Africa; “unprecedented development of several classes of new antiviral drugs” — the first of which, AZT, killed (conservatively) 150,000 people, while the later ones have not extended life-spans; “we have gained remarkable insight into this new pandemic” — but don’t understand how “HIV” causes death of CD4 cells nor what might provide immunity, and we administer drugs that don’t extend lives and cause death by organ failure.
Every indication is that this was written carelessly, perhaps hurriedly, and without proper checking of the cited references. No matter why, it’s a shoddy piece.
This entry was posted on 2008/10/16 at 3:30 pm and is filed under antiretroviral drugs, experts, HIV skepticism. Tagged: Gay-Related Intestinal Dysbiosis, mistaken Nobel Prize, Nobel Prize for HIV discovery; unwarranted Nobel Prize, Tony Lance. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.