by Liam Scheff
What is AIDS
“Previously Healthy Young Gay Men”
Drugs, STDs and Antibiotics, not Sexual Identity
In no time, the medical authorities cast the “AIDS” diagnosis over a wider group of drug users – including heroin addicts, and then expanded it to Hemophiliacs, and then the poorest of the poor Africans. So, AIDS became any illness in “populations at risk.” But, “at risk” for what? “At risk for AIDS!” is the answer. And we have our second circular definition in the AIDS campaign.
LAV, er, HTLV-iii, um, “HIV” Loves, em, Kills? T-Cells….
“Until recently, prevailing dogma said HIV causes AIDS by killing T-cells. Most people, including Robert Gallo, still adhere to this belief even though there is no evidence to support it. On the contrary, the wealth of evidence available clearly shows that HIV does not, in fact, kill T-cells. This is not surprising since the hallmark of retroviruses (HIV included) is that they do not kill cells [1, 2].The discoverer of HIV, Luc Montagnier, heads  a list [4-6] of virologists who have confirmed that HIV does not kill T-cells in culture. Neither does it kill T-cells in human beings. Mario Roederer of Stanford University said in an editorial in 1998  that the results of Pakker et al.  and Gorochov et al.  “provide the final nails in the coffin for models of T cell dynamics in which a major reason for changes in T cell numbers is the death of HIV-infected cells.”[...]The fact that HIV does not kill T-cells has caused a remarkable about-face in mainstream thinking. Commenting on a recent paper by Hellerstein et al. , Guido Silvestri and Mark Feinberg summarized in 2003 the latest speculation that HIV causes AIDS not by killing T-cells but by over-stimulating the immune system . Silvestri and Feinberg inform us that, “Prevailing views…have shifted from models that focus primarily on direct HIV-mediated killing of CD4+ T cells to models that emphasize the pathogenic role of generalized immune system activation.” In other words, HIV no longer causes AIDS by killing our immune cells, as Gallo contends, but by boosting our immune system.” Rethinking Aids.com/Gallo Rebuttal
Dear Experts, How Does “HIV” Smash Up T-Cells?
Indirect mechanisms of HIV pathogenesis: how does HIV kill T cells?Although twelve years have passed since the identification of HIV as the cause of AIDS, we do not yet know how HIV kills its target, the CD4+ T cell, nor how this killing cripples the immune system. Prominent theories include direct killing of infected CD4+ T cells by the action or accumulation of cytopathic viral DNA, transcripts or proteins, or by virus-specific cytotoxic T lymphocytes, and indirect killing of uninfected CD4+ T cells (and other immune cells) by autoimmune mechanisms, cytokines, superantigens, or apoptosis. In the past year, studies have provided tantalizing clues as to why infected cells may not die and how these infected cells kill innocent bystander cells. [LINK]
“Life-Saving” Life-Ending Drugs
“Prevailing views concerning the pathogenic mechanisms of AIDS have shifted from models that focus primarily on direct HIV-mediated killing of CD4+ T cells to models that emphasize the pathogenic role of generalized immune system activation. The observation that increases in T cell turnover seen in HIV-infected individuals primarily reflect increased proliferation of effector-memory T cells supports the concept that chronic immune activation plays a prominent, if not predominant, role in the pathogenesis of AIDS.” [LINK]
Exosome, Not HIV
“The National Institutes of Health (NIH) reported that retroviruses ‘are so irregular and so labile that we have been unable to apply the tools of structural analysis to good effect.’ It also reported that retroviral DNA ‘closely resembles a cellular mRNA’ messenger vesicle. Retroviruses are also said to be ‘unique among animal viruses in that some groups exhibit considerable polymorphism in receptor usage.‘ They are thus particularly well suited for carrying messages – as they can deliver ‘irregular’, or varying, code ‘similar to’ mRNA to many kinds of cellular receptors.” [LINK]
“The continuing mystery of retroviral structure reflects less a lack of will—or skill—on the part of researchers than on a quirk of nature. Mature virions are so irregular and so labile that we have been unable to apply the tools of structural analysis to good effect.” [LINK]
“Retroviruses are unique among animal viruses in that some groups exhibit considerable polymorphism in receptor usage among otherwise closely related viruses.” [LINK]
Retroviruses Are Exosomes, and so is “HIV”
“Hildreth now proposes that “the virus is fully an exosome in every sense of the word.” Others have found that HIV particles contain MHC, but by the exosome hypothesis they may also contain proteins that exosomes use to fuse with target cells and to avoid attack by complement. As Gould points out, an exosome makes a perfect vector for HIV, because an exosome “is not just proteins in a vesicle, it’s something that is meant to traffic.” [LINK]
“To block all entry, suggests Hildreth, perhaps the MHC should be the target. Alloimmunization—immunization with a wide range of MHC and other protein variants (e.g., by injecting killed leukocytes)—might allow a newly infected individual to mount a quick attack on the incoming HIV, which is packed with foreign MHC. Gould even suggests, “this is why we have tissue rejection responses— [they evolved] to protect us from retroviruses.” He points out that alloimmunity predates and thus could not have arisen from adaptive immunity.”
“The more extreme idea of xenoimmunization does work in monkeys, which can reject SIV grown in human cells. And for Thomas Lehner (Guy’s Hospital, London, UK), who has been pushing the idea for several years, alloimmunization “is far better than anything we have at the moment.” But it has languished since the monkey experiment, perhaps based on fears that it would prevent later transplants, cause rejection during pregnancies, and fail to catch a handful of HIV particles before they replicate and thus incorporate self-MHC.”
Why the Hysteria?
When “AIDS” was “Cancer”
Save the Exosomes!
2. Weiss R, Teich N, Varmus H, Coffin J. Molecular Biology of RNA Tumor Viruses. Plainview, NY: Cold Spring Harbor Lab. Press; 1985.
3. Lemaitre M, Guetard D, Henin Y, Montagnier L, Zerial A. Protective activity of tetracycline analogs against the cytopathic effect of the human immunodeficiency viruses in CEM cells. Res Virol 1990,141:5-16.
4. Langhoff E, McElrath J, Bos HJ, et al. Most CD4+ T cells from human immunodeficiency virus-1 infected patients can undergo prolonged clonal expansion. J Clin Invest 1989,84:1637-1643.
5. Anand R, Reed C, Forlenza S, Siegal F, Cheung T, Moore J. Non-cytocidal natural variants of human immunodeficiency virus isolated from AIDS patients with neurological disorders. Lancet 1987,2:234-238.
6. Hoxie JA, Haggarty BS, Rakowski JL, Pillsbury N, Levy JA. Persistent noncytopathic infection of normal human T lymphocytes with AIDS-associated retrovirus. Science 1985,229:1400-1402.
7. Roederer M. Getting to the HAART of T cell dynamics. Nature Medicine 1998,4:145-146.
8. Pakker NG, et al. Biphasic kinetics of peripheral blood T cells after triple combination therapy in HIV-1 infection: a composite of redistribution and proliferation. Nature Medicine 1998,4:208-214.
9. Gorochov G, et al. Perturbation of CD4+ and CD8+ T-cell repertories during progression to AIDS and regulation of the CD4+ repertoire during antiviral therapy. Nature Medicine 1998,4:215-221.
10. Grossman Z, Herberman RB. T-cell homeostasis in HIV infection is neither failing nor blind: modified cell counts reflect an adaptive response of the host [see comments]. Nat Med 1997,3:486-490.
11. Hellerstein M, Hanley MB, Cesar D, et al. Directly measured kinetics of circulating T lymphocytes in normal and HIV-1-infected humans [see comments]. Nat Med 1999,5:83-89.
12. Hellerstein MK, Hoh RA, Hanley MB, et al. Subpopulations of long-lived and short-lived T cells in advanced HIV-1 infection. J Clin Invest 2003,112:956-966.
13. Silvestri G, Feinberg MB. Turnover of lymphocytes and conceptual paradigms in HIV infection. J Clin Invest 2003,112:821-824.