In April 1986, Dr. Knox stated in an interview with the New York Native: “We’re finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB.”140 Knox said she believed that HIV kind of acts as a “wet nurse” to HHV-6A.
Knox and Carrigan found that every AIDS patient had active replication of HHV-6A in every stage of AIDS, from their diagnosis to their autopsies, with many having CD4+ cell counts over 700. With HHV-6A, there were none of the bewildering questions about how a seemingly benign retrovirus could possibly cause all that carnage. “It’s also much more destructive. . . . It kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow.” When New York Native interviewer Neenyah Ostrom asked Knox, “Can HHV-6A do everything that HIV can do?” Knox gave this chilling answer: “As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV.”141 Citing data from multiple studies by diverse scientists, Knox added: “Where we have seen HHV-6A in tissue, we see dead tissue. And where you see . . . HIV alone . . . you don’t see dead tissue. You don’t see destroyed organs and scar formation, and that’s what you see when you see HHV-6A. We find replacement of the normal architecture of the lymph nodes with scar tissue. HHV-6A kills it. It kills the lymph node tissue.”142
Knox parroted the obligatory language that HHV-6 was acting in concert with HIV. That language would preserve her from reputational and financial suicide. “I think they’re a team. And, when the two of them are present, they induce the production of more of each other. It’s a mutually enhancing relationship. It’s our feeling that if you could interrupt or limit or suppress the HHV-6A infection, the levels of HIV would go down tremendously, and HIV would become just a chronic viral infection. . . . We don’t have any evidence, looking in the tissue, that HIV is responsible for any of the destruction. And, if you think about it, HIV infects patients for years—a decade or more—without progressing to AIDS. When you look in their tissues, you have to ask how you can have such a long-term viral infection and have no damage?”143
NIH quickly cut off funding for Knox and for anyone else who wanted to research HHV-6. When Neenyah Ostrom asked, “Why can’t you get more funding for this research?” Knox replied, “Well, I don’t know if you’ve been tracking the kinds of exposés that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there’s been a real resistance to entertaining hypotheses or directions of AIDS research that aren’t looking specifically at HIV, and that is the basic problem. Our studies themselves have been enthusiastically received, but the funding hasn’t followed. And that is funding through the federal agencies—like the NIH.”144
That summer, Italian researcher Dario Diluca published his findings in the Journal of Clinical Microbiology, reporting HHV-6 in the lymph nodes of 22 percent of Chronic Fatigue Syndrome patients and only 4 percent of healthy people. This research raised the possibility that AIDS, which affects gay men, is the same disease as CFS, which became widespread in heterosexuals and in virtual lockstep with AIDS in the early 1980s.145
Surveys of CFS patient groups in thirty-five states show an exponential rise in cases produced each year since the 1970s. This curious temporal and case production relationship with the AIDS epidemic prompted many researchers to characterize CFS as an AIDS epiphenomenon. Gallo’s discovery and Knox’s revelations suggested that the new human herpesvirus HHV-6 might be a critical causative cofactor shared by both AIDS and CFS. In June 1989, CFS research pioneer Dr. Paul Cheney, PhD, MD, testified before Congress that CFS might have a relationship with the AIDS epidemic.146 In January 1993, six months after the Amsterdam conference, Dr. Anthony Komaroff at Harvard University and his coworkers published a study that showed that brain lesions developed in CFS patients who had Human Herpes Virus-6 active in their bodies.147
Such revelations could only have terrified Tony Fauci. Ever since the 1992 Amsterdam meeting, Dr. Fauci had been insisting that CFS was a psychosomatic disease. The suggestion that it might be related to AIDS threatened the entire HIV paradigm.
In their 1988 “natural killer cells” paper, Lusso and Gallo had quietly disclosed that they had found HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. “They identified the problem in both sets of patients,” said Knox, “so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.”148 When Gallo and Lusso conducted a trial treating half their AIDS patients with acyclovir—a remedy against herpes—and half with AZT alone, they found a significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone.149
Said Knox, “In laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than [AZT], and if you’re talking about treating healthy people in a clinical trial, you’re looking for something that people can take orally.”150
These kinds of findings threatened to derail and discredit Anthony Fauci’s entire HIV/AIDS paradigm. What, after all, would be the implications if a mild, off-patent remedy like acyclovir could safely treat AIDS more effectively than Dr. Fauci’s expensive pharmacopoeia of deadly chemotherapy poisons? He choked off any further funding for HHV6 research, despite Knox’s potentially lifesaving discovery of the efficacy of acyclovir against AIDS.
Mycoplasma
Dr. Shyh-Ching Lo, the Chief Researcher in charge of AIDS programs for the Armed Forces Institute of Pathology, was one of the many researchers baffled by Anthony Fauci’s unconventional claim that antibodies—heretofore the signal of a robust immune response—should, uniquely with HIV, instead be the signal for impending death. That was a bridge too far for Dr. Lo: he took the conventional position that the presence of the antibodies to HIV—far from being a sign of doom—is proof that the body has coped successfully with the virus.
“There is no good explanation for why and how the virus breaks out of the antibody protection,” complained Dr. Lo.151,152 “I’m not saying that HIV plays no role in AIDS—the data shows a clear correlation with disease.” He recited the mandatory disclaimer: “But AIDS is much more complicated than HIV.”