Letter to the Editor:
Response to Zhu et al. 1959 Origin of AIDS
Leonard G. Horowitz, D.M.D.,M.A.,M.P.H.
Tetrahedron Publishing Group
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The politically correct analysis applied to Zhu et al.’s speculative findings published in “An African HIV-1 sequence from 1959 and implications for the origin of the epidemic,” was unbecoming of Nature (February 5, 1998). The authors concluded that four genetic fragments isolated from the blood of an African man in 1959, “authenticate this case as the oldest known HIV-1 infection.” They added that the genetic sequences suggested that “all major [HIV] group viruses, may have evolved from a single introduction into the African population not long before 1959.(1)
Albeit the Pasteur Institute’s Wain-Hobson proposed (in the same issue) that the Zhu et al. “data are limited [and] we’re in the realm of speculation, meaning that the story is not over.” To state, however, that “the collapse of European colonialism,” that is, the end of largely British military rule over Africa, resulted in “changes in urban and technological traits” that prompted such “emerging microbial infections,” speculates beyond scientific plausibility. Though historically accurate and politically correct, the statement implies that dirty Black Africans brought new plagues upon themselves, or through God’s wrath, when cleaner white Englishmen were driven from their territorial possessions.(2)
Another objectionable conclusion was spun by the Zhu et al. team leader David Ho in the study’s heralding article in The New York Times (3). His group’s findings, Ho claimed, put an end to the theory that the AIDS virus was engineered in American biological warfare laboratories by Pentagon contractors–a theory initially advanced by a British medical scholar, John Seale, though Ho falsely accused Russian spin doctors for the alleged hoax.(4)
Although American newspapers trumpeted Zhu et al.’s “1959 AIDS Case” discovery (5), “it is not known if the man died of AIDS,” Lawrence Altman clarified in NYT.(3) The adult Bantu male may have died of sickle cell anemia for which his glucose-6-phosphate-dehydrogenase enzyme deficiency was being genetically studied at the time.
Political agendas aside, what then did Zhu et al. really find? More importantly, how might their findings be reinterpreted to better elucidate AIDS’s origin?
Questionable Background and Methods
Historically, this “case” and blood sample had raised questions. Nahmias et al. allegedly found HIV-1 in this one of 1,213 Leopoldville blood samples.(6) These samples had been available for more than a quarter century, that is, from the 1950s when large scale polio vaccine trials were also underway in Leopoldville. Following publication of their study, however, the sample was said to have been lost.(7) Thus, confirmatory studies could not be undertaken.
For Zhu et al. this sample fortuitously reappeared. From it they extracted viral RNA. “As it turned out,” wrote Wain-Hobson, “the HIV genomic RNA was substantially degraded, meaning that, after much labour, the authors could obtain only a few 300-nucleotide fragments of DNA.” Then “multiple primers [additional RNA sequences] were used [i.e., mixed in with the original isolated fragments] in a single RT [reverse transcriptase initiated] reaction, and all synthesized complementary DNAs were amplified by PCR [polymerase chain reaction] using primers designed to amplify HIV-1 sequences from all known subtypes. . . . This mixture was heated to 70 degrees C for 10 minutes and used to synthesize HIV-1 cDNA . . . Each PCR product was then purified, cloned and sequenced.
The “synthesized” sequences of HIV, the authors stated, allowed “ample [genetic] comparisons” and the construction of family trees reflecting the evolution of the virus and its relatives.
Certainly such methods and materials should bare scrutiny. Common sense begs to know how HIV-1, composed of several genes including the LTR, gag, pol, nef, and env portions, and a few smaller ones sprinkled in, could be honestly “synthesized” from four degraded fragments of just two of these, the pol and env, genes? The four fragments were manipulated, the authors described, then labeled ZR59a, b,c, and d. They said these compared very closely with the GenBank data base. There was only a “0-3% divergence. . . . [and] maximum sequence identity scores of 92% (ZR59a), 96% (ZR59b), and 94% (ZR59c) confirmed that the ZR59 sequences are indeed unique and unlikely to be the result of PCR contamination.”
The uniqueness of these segments should also be questioned. Moreover, if not the result of PCR contamination, what about vaccine contamination?
The authors failed to report that the sequences may not have been unique to the AIDS virus alone. The theory that these fragments might have originated in contaminated polio vaccines, and may have, like the AIDS virus, been the result of vaccine initiated viral recombination(s) has been periodically advanced.(8) The Zhu, Ho et al. study was uncontrolled in this respect, and obviously not double blind. They failed to compare their ZR59 fragments with numerous other viruses that were likely to have contaminated the blood of Central African villagers including this Bantu man. It is possible the ZR59 sequences might have similarly compared to other blood borne pathogen sequences including common polio vaccine contaminants such as simian foamy retroviruses containing reverse transcriptase, the herpes type viruses–herpes B, Epstein Barr, simian cytomegalo–SV40, and others.
This being the case, had Zhu et al.’s short fragments of RNA come from other viruses inoculated into this Bantu man during vaccine trials, then given their study methods, similar results, but not conclusions, might be obtained. In this case, HIV could not be considered a human or monkey virus, but an iatrogenic primate hybrid dating back only to mid-1950s or even 1960s. Then the authors’ conclusion that “the major-group viruses that dominate the global AIDS pandemic at present shared a common ancestor in the 1940s or early 1950s” would be misleading. Evidence for this obvious weakness in their report came directly from the authors when they reported that “[i]f ZR59 were a result of a recombination of the B and D subtypes [of the AIDS virus] . . . the recombination would be unlikely to be detectable, especially with the short sequences available.”
Moreover, had biological weapons contractors isolated such a mutant during the early 1960s, then Dr. Seale’s politically objectionable hypothesis might be accurate. Reprinted U.S. biological warfare contractor documents prove that immune system ravaging hybrid viruses were being isolated, recombined, and tested at least as early as 1962. By 1971 they included retroviruses functionally similar, if not identical, to HIV-1.(8)
Vaccine Contamination: A Politically Incorrect Perspective
Had the polio vaccine viral recombinant theory been discussed by Zhu et al. it might have provoked, in the words of oral polio vaccine (OPV) pioneer Albert Sabin “another obfuscation” for the vaccine industry.(8) Sabin’s expressed desire to withhold evidence that his polio vaccine was riddled with carcinogenic viruses came as massive efforts to distribute contaminated OPV was underway in the United States, Africa, and Russia. Rather than expressing such concerns Zhu et al. hedged their discussion writing, “the factors that propelled the initial spread of HIV-1 in central Africa remain unknown: the role of large-scale vaccination campaigns, perhaps with multiple uses of non-sterilized needles, should be carefully examined, although social changes such as easier access to transportation, increasing population density and more frequent sexual contacts may have been more important.” Notice not a word about contaminated vaccines. Nor was the inherent risk of in vitro and in vivo viral recombination(s) addressed.
A curious association advanced by the authors was that “[f]or most regions of the HIV-1 genome, subtypes B and D are more closely associated with each other than are any other subtypes with the major group.” Of the six major AIDS virus subtypes, the B subtype is most common to North America. The D subtype is most common to Uganda, and the F subtype is most common in Zaire.(9) The authors’ analysis showed an “unusual B/D/F clustering found in [their] phylogenetic analyses.” Given the administration of contaminated monkey kidney tissue derived polio vaccines in these areas from the mid 1950s through the 1960s; and later, the testing of contaminated hepatitis B (HB) vaccines in these specific areas during the late 1960s through mid-1970s, the B, D and F subtypes may have closely evolved in experimental subjects, or in the vaccines given them. Critically relevant is the fact that these early experimental hepatitis B vaccines were tested in these areas of the world, and in the populations most plagued by AIDS.(10) These four subtype HB vaccines were partially processed in live contaminated chimpanzees housed in New York City where biohazard and containment problems were reported.(11) After growth in contaminated chimpanzees, live HB viruses were inoculated into human subjects whose blood serum was then taken to develop 200,000 doses including four subtypes of the HB vaccine administered by 1974.(10) The close link between HIV-1 and chimpanzee SIV is well established, and might be best explained in this manner.(12)
Thus, Zhu et al.’s speculation that “all major [HIV] group viruses may have evolved from a single introduction into the African population not long before 1959″ may be misleading. The virtual simultaneous administration of contaminated polio vaccines, followed by the testing of four different contaminated HB vaccine subtypes, containing human/chimpanzee recombinant viruses, offers an alternative if not more plausible explanation. Contaminated vaccine theories pertaining to the origin of AIDS are at least as plausible as other theories including: “multiple uses of non-sterilized needles,” “social changes such as easier access to transportation,” “increasing population density,” and/or “the collapse of European colonialism.” Clearly, these factors were largely, if not completely, inconsequential to the North American outbreak.
Leonard G. Horowitz, D.M.D., M.A., M.P.H.
1) Zhu T, Kober BT, Nahmias AF, Hooper E, Sharp PM, and Ho DD. An African HIV-1 sequence from 1959 and implications for the origin of the epidemic. Nature 1998;391;Feb 5;594-597.
2) Wain-Hobson S. 1959 and all that. Nature 1998;391;Feb 5;531-532.
3) Altman L. Family tree shows AIDS developed a decade earlier. New York Times 1998, Wednesday, Feb 4, p. 23.
4) The Russians also acknowledged Seale’s pioneering thesis in: Moscow World Service in English. Belitskiy on How, Where AIDS Virus Originated. March 11, 1988. Published in International Affairs. FBIS-SOV-88-049, March 14, 1988, p. 24.
5) Associated Press Staff. 1959 AIDS Case discovery. As published in Ft. Lauderdale, FL: Sun Sentinel. Wednesday, Feb 4., 1998, p. 12.
6) Nahmias AJ, et al., Evidence for human infection with an HTLV-III/LAV-like virus in central Africa, 1959. Lancet 1986;i;1279-1280.
7) Garrett L. The Coming Plague: Newly Emerging Diseases in a World Out of Balance. New York: Penguin Books, 1994, pp. 371-81.
8) Horowitz LG. Emerging Viruses: AIDS & Ebola–Nature, Accident or Intentional? Tetrahedron, LLC, 1998, pp. 127-134; 403-463; for Albert Sabin’s concerns see p. 484 and primary source–an audiotaped interview with Maurice Hilleman by Edward Shorter for The Health Century (1986), PBS documentary series on file at the National Library of Medicine, Bethesda, MD.
9) Myers G. et al. “Phenogenetic moments in the AIDS epidemic,” Chapter 12 in S. S. Morse, ed., Emerging Viruses. Oxford, Eng.: Oxford Univ. Press, 1993.
10) Horowitz LG. Op cit., pp. 253, 497. For original documentation regarding the chimpanzees used to culture four subtypes of HB viruses for vaccine trials in different parts of the world including New York City and Central Africa in 1974 see: Purcell RH. Current understanding of hepatitis B virus infection and its implications for immunoprophylaxis. In: Antiviral Mechanisms: Perspectives in Virology IX. The Gustav Stern Symposium. New York: Academic Press, 1975, pp. 49-76.
11) Krugman S. Viral hepatitis type B: Prospects for active immunization. In: International Symposium on Viral Hepatitis, Milan, Dec. 1974. Develop. biol. Standard. Vol. 30 Munich: S. Karger Basel, 1975, pp. VI; 363-367; 375-379.
12) Schulz TF. Origin of AIDS (letter to the editor) Lancet 1992;339:867.