The gay press glossed over urgent medical warnings from scientists about the dangers of poppers. The Advocate, a popular US magazine for homosexuals, refused to print letters from dissident scientists like Duesberg while accepting parades of poppers advertisements from Great Lakes Products, the era’s largest manufacturer of sex drugs. Those advertisements exonerated poppers from any connection to AIDS, openly declaring them harmless.131 Pharmaceutical companies including Hoffmann-La Roche invested money in the gay community with innumerable advertisements for AIDS medications. Burroughs Wellcome ran an ad for poppers calling amyl nitrite (i.e., poppers) “the real thing.” Gay publications and organizations continued to promote poppers and censure stories about their health risks.132
His historical cultivation of relationships with gay leaders was one of the factors that made Dr. Fauci a darling of liberals during the early COVID crisis. Numerous other historical and personal factors induced liberals to accept Dr. Fauci without scrutiny. Blind faith in Saint Anthony Fauci may go down in history as the fatal flaw of contemporary liberalism and the destructive force that subverted American democracy, our constitutional government, and global leadership.
Deadly Viruses and Mycoplasma
As the HIV/AIDS hypothesis came under attack for its many discrepancies and internal contradictions, scientists besides Duesberg were discovering bugs that provided more plausible culprits in the AIDS pandemic.
Among these competing hypotheses were two advanced, individually, by Robert Gallo and Luc Montagnier. It’s probable that diplomacy, self-interest, and honed survival instincts prompted both men to introduce their pathogens as “cofactors” that might work alongside HIV to trigger AIDS. Critics pointed out that the new pathogens these scientists uncovered were so clearly deadly on their own that they hardly needed HIV; the discovery of these genuinely lethal germs made HIV superfluous and redundant to explaining the pandemic. But for these gentlemen, it was obligatory to genuflect to the inviolable orthodoxy that anointed HIV as AIDS’s ultimate cause. They may, in fact, have seen their discoveries as salvatory of the original HIV hypothesis. It was becoming increasingly challenging to credibly claim that HIV, which remained dormant for decades within its host, could somehow suddenly become virulent—“the most deadly disease in history”—without some external provocation.
HHV6
In 1986, Robert Gallo announced the discovery of human herpesvirus (HHV6). This new pathogen was no benign retrovirus. It was instead a savage cell-killing DNA virus. Gallo’s lab had found the murderous HHV6 “killer cells” in the blood of AIDS-infected men and in patients suffering from Chronic Fatigue Syndrome (CFS), an immune deficiency disease extremely similar to AIDS, that had appeared in heterosexuals on the exact same timeline as AIDS appeared in homosexuals. Many critics already suspected the two diseases were one and the same. Gallo’s discovery seemed to fortify that supposition.133
In a 1995 article titled “Human herpesvirus 6 in AIDS,”134 Gallo says, “HHV6 may act as an accelerating factor” in HIV infection because “HHV6 can also infect and kill CD8+ T-cells, natural killer cells, and mononuclear phagocytes,” all major components of the immune system. Ironically, Gallo’s discovery of HHV6 might have won him the Nobel Prize if he hadn’t jumped the gun a decade earlier by stealing HIV from Montagnier. None of the embarrassing questions about how in the world the seemingly benign HIV retrovirus could cause deadly disease bedeviled his lethal new killing machine.
While HIV was never shown to be cytocidal, HHV6 had a murderous affinity for CD4 and T-cell “in potential effects on the immune system and brains.” Gallo declared that HHV6 was a major source of disease progression in AIDS.135,136
On May 11, 1988, the Miami Herald reported Gallo’s announcement: “A newly discovered highly contagious herpes virus might play a role in causing several types of cancer and could be a co-cofactor in wiping out the immune systems of AIDS patients, one of the nation’s premier virologists [Robert Gallo] said Tuesday.”137 The Herald also wrote, “Since the AIDS virus kills only a small percentage of T-4 cells at a time, Gallo said the new herpes virus [HHV-6], if proven to be the co-cofactor, could explain the total annihilation of T-4 cells in AIDS patients. ‘The virus kills cells after using them to replicate,’ he said.” The Herald quotes Gallo as saying, “So if a co-cofactor is involved in the development of AIDS, and I’m not convinced it’s absolutely needed . . . then we want to consider this one strongly.”138
Charles Ortleb told me that Gallo’s study “struck me as being backwards. If Gallo’s new DNA virus explains the ‘total annihilation’ of T-4 cells, why would it need a cofactor? The ‘cofactor’ in this mystery would have to be HIV, not HHV-6.”
Some scientists had similar reservations. HHV6 didn’t seem to need a retrovirus wingman. Duesberg remarked dryly that to the extent that Gallo’s newly discovered pathogen was “partnering” with HIV, then HHV6 was the senior partner in the collaboration. I can’t help wondering if it occurred then to Gallo that if only he had not impetuously stolen Montagnier’s discovery four years earlier, he might have collected his long-sought Nobel for his own authentic discovery of a much more plausible AIDS virus. Alas, it was not to be. But Dr. Fauci had committed his agency to the HIV hypothesis. And Gallo had built his career on HIV—even if he stole it from Montagnier, says Charles Ortleb. “When Gallo began that battle with Fauci,” says Ortleb, “the agency was already fully committed to the HIV theory and could not afford any signs of retreat.” I asked, “Why would Gallo not pull rank?” Ortleb answered, “Gallo is a classic sociopath. He knows that his survival means acquiescing to Fauci.”
Following Gallo’s “natural killer cells” article, other researchers confirmed the links between HHV6 and AIDS. In 1996, Konstance Knox, PhD, and Donald R. Carrigan, PhD, published a study demonstrating that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6A infections in their lymph nodes early in the course of their disease.139 This finding led Knox and Carrigan to conclude that “active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS.”