Gallo’s failed application for a Nobel Prize
Posted by Henry Bauer on 2013/08/12
Reading some stuff from the early days of AIDS, I came across the “Review Article” by Wong-Staal and Gallo, “Human T-lymphotropic retroviruses” (Nature, 317  395-403).
The piece qualifies for scare quotes around Review Article because it’s actually just blatant self-promotion by way of assertions that are, to say the very least, dubious.
Thus Gallo is credited (credits himself) with discovering the “first human retroviruses”, HTLV-I and HTLV-II which are asserted causes of adult-onset leukemia (ATL), in which T-cells proliferate cancerously.
He is also credited with the discovery of HTLV-III, which was later re-named HIV as a compromise after it had been established conclusively to have been a clone of Montagnier’s LAV. Perhaps to discount further Montagnier’s claim to priority, “Subsequent studies demonstrated that . . . [HTLV-I and HTLV-II] were closely related to the LAV isolate”.
Gallo’s claim to priority is also stated quite explicitly: “The idea and the approach to the identification of a unique human T-lymphotropic retrovirus in AIDS is largely derived from epidemiological data and from studies on HTLV-I. The idea was first proposed by R.C.G., based on several considerations derived in part from discussion with M. Essex”.
HTLV-III is asserted to be kin to HTLV-I and HTLV-II because they all affect T-cells, even though III does the opposite from what I and II do: it kills cells rather than causing their proliferation. To further underscore that they are all in the same family of (Gallo-discovered) human retroviruses, we are told that “the term HTLV-III does not depend on an arbitrary extent of nucleotide sequence homology to HTLV-I and HTLV-II” — in other words, biological kinship is not decided on the basis of genetics!? When it is genetics that determines kinship in all other realms of biology? And in what way was LAV then “closely related” to the HTLVs?
On the other hand, it is asserted that “Molecular clones of the genomes of all three subgroups of HTLV have been obtained [references 82-88] and the complete nucleotide sequence of one or more isolates of each subgroup has been published [references 89-95]”.
It’s a nice trick, it seems to me, to get the compete genomes of entities that have never been isolated in pure form. How do you molecularly clone something that is not a pure substance?
But then Gallo asserted as late as 2006, in his testimony in the Parenzee trial in Australia, that because he could make a lot of virus therefore purification was not needed:
“Once we could mass-produce this virus, that’s purification. If you have a tonne of something and you contaminate it by a drop of water, didn’t you purify it? . . . . virus comes out in great quantity and forever, thus making purification already accomplished” (p. 1278); “mass-produced virus . . . by itself is purified virus” (p. 1281 of Parenzee trial transcript).
Gallo’s idiosyncratic attitude toward purification seems even more remarkable given that his “review” mentions “the heterogeneity of different HTLV-III isolates”. Of course they’re heterogeneous, since they contain all sorts of stuff because the purported “HTLV-III” was never separated from the other material. Biologists should surely be as aware as are other scientists of the possible effects that even the tiniest contamination might exert, since those contaminants might be catalytic (or enzymatic) in their action — see “Purify? Who needs that? (So says Robert Gallo)”.
Assertions of which I was previously unaware include that “the leukemia virus (HTLV-I) can also cause immunosuppression and opportunistic infections, and it is possible that the immunosuppressive virus (HTLV-III or lymphadenopathy-associated virus, LAV) can cause leukemia once its cytopathic property is blocked”. “HTLV-I and HTLV-II also showed immune suppressive activity in vitro and . . . [there were] opportunistic infections in ATL patients”; “properties of HTLV-I are limited manifestations of the more profound immunosuppressive and cytopathic properties of HTLV-III”. In a similar vein, in his autobiography Gallo asserts that HTLVs I and II are “the only known specific co-factors for AIDS” (emphasis in original, p.
248 in Gallo’s autobiographical Virus Hunting: AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery, Basic Books, 1991).
Another assertion of similarity is that all three HTLVs have similar modes of transmission: “sexual, congenital and blood”. It seems odd to lump congenital transmission, which surely means hereditary, endogenous, with the other two, which function via exogenous infective agents. Gallo continued to make this puzzling assertion for many years; it appears also in his autobiography (p. 114 in Virus Hunting): “HTLV-I, ‘tended to be transmitted within families and to stay within families for generations’”.
I found it interesting to read that antigens of HTLV-I cross-react with those of “the AIDS agent”, in other words that “HIV” tests were known from the very beginning to be not specific to HIV. Also interesting was the assertion that HTLV-III “is only indirectly involved in . . . Kaposi’s sarcoma . . . as viral genetic information is . . . not detectable in Kaposi tunor . . . . [which] can occur in the absence of any apparent T-cell defect”: So it was also known from the very beginning that Kaposi’s sarcoma, originally iconic of “AIDS”, had nothing to do with immune deficiency or presence of HIV.
The assertion of observed cell-killing in vitro by HTLV-III was contradicted later in Montagnier’s lab, where it was found that the cell-killing agent could be inactivated by antibiotic and was therefore probably a mycoplasma and not a virus: Lemaître et al., “Protective activity of tetracycline analogs against the cytopathic effect of the human immunodeﬁciency viruses in CEM cells”, Research in Virology, 141 (1990) 5-16; “Role of mycoplasma infection in the cytopathic effect induced by human immunodeﬁciency virus type 1 in infected cell lines”, Infection and Immunity, 60 (1992) 742-8.
I noted that with “HTLV-III, infection is followed by persistence of unintegrated . . . DNA”, recalling that Etienne de Harven has pointed out that such random circulating DNA could give rise to positive “HIV” tests — “Human Endogenous Retroviruses and AIDS Research: Confusion, Consensus, or Science?”, Journal of American Physicians and Surgeons, 15 (#3, 2010) 69-74, .
And this “Review” repeats the optimistic view expressed in the notorious press conference of April 1984: “Recent demonstrations of neutralizing antibodies in AIDS and pre-AIDS patients . . . are encouraging for the prospects of a vaccine” — prospects that remain nothing beyond prospects even some 3 decades later.
This not-so-subtle attempt to come to the attention of the Nobel Committee culminates in Table 1, where similarities between HTLVs I and II and III are listed, together with asterisked items supposed to be unique to Gallo’s HTLVs, including that they are human, exogenous, infectious retroviruses; show particular T4 tropism; that there are highly related viruses (STLV-I, STLV-III) in Old World monkeys; as well as some technical aspects of the genome.
That this article appeared in Nature says things not only about that journal’s claim to pre-eminence but also about the nature of peer review and its purported role in safeguarding the quality of the scientific literature. Much of what I criticize here required no later knowledge to understand its flaws. For a fully documented analysis of the misdeeds of Gallo’s laboratory, see John Crewdson’s Science Fictions: A Scientific Mystery, a Massive Cover-Up, and the Dark Legacy of Robert Gallo (Little, Brown, 2002). Gallo was spared the ignominy of a finding of scientific misconduct only by administrative intervention: “HHS: Gallo Guilty of Misconduct “Federal inquiry finds misconduct by a discoverer of the AIDS Virus” (Science, 259  168-70); “Excerpts from conclusions of report of the Office of Research”; “Report found scientific misconduct”.