reply to post by SaturnFX
I'm a Ph.d in virology and microbiology.
I am not a retrovirologist, H.I.V. is a retrovirus, I am whats known as a BSL-3 & 4 virologist.
I have worked with H.I.V. and S.I.V. though however for 18 months, a full year of that time was spent helping out a friend who is self funded.
The conclusion that I came to on the subject, is that H.I.V. is NOT the cause of the syndrome known as A.I.D.S..
I agree with Duesberg on the subject 210%.
H.I.V. is not even nessesary for A.I.D.S., H.I.V. free A.I.D.S. is called "Idiopathic CD-4-lymhocyopenia" or simply just (ICL) its not even reported
to CDC anymore.
Before the 1985 press conference given by Dr. Robert Gallo, and held by the Secretary oF Health and Human Services at the time (MARGRET HECKLER)
announcing the H.I.V. virus, which at the time was known as
HTLV-III, A.I.D.S. in Africa was simply calked uP to malnutrition by rats like Dr. Anthony Fauci.
Gallo & Fauci both are nothing but total money grubbing frauds, under no uncertain terms. Fauci swept "ICL" completely under rug with the most
ignorant tripe filled crap explanation that ANYONE could ever even possibly imagine, never to be mentioned again. >ROME HAS SPOKEN--->CASE CLOSED
Take a look at number 4 in the below link.
A copy of the NIH reply to the above letter is avalible upon request at the CDC website, its called the "DONNA E. SHALALA" letter.
If your interested I can show you more than just a few things, starting with this here below ?
*HIV ASSUMED TO KILL T-CELLS*
Based on early observation by Gallo et al., HIV is assumed to cause immunodeficiency by spcifically killing T-cells (Gallo et al., 1984; Weiss and
Jaffe, 1990). Gallo observation was restricted to primary T-cells (Gallo et al., 1984) but not established T-cell lines (Rubinstien, 1990) However,
according to Montagnier, the discoverer of HIV, "In a search for a direct cytopathic effect of the virus on (primary) T-lymphocytes, no gross changes
could be seen in virus producing cultures, with regard to cell lysis or impairment of cell growth" (Montagnier et al., 1984). Others have confirmed
that HIV does not kill infected, primary T-cells in vitro (Hoxie et al., 1985 Anand et al., 1987 Langhoff et al., 1989 Duesberg, 1989c). Moreover,
HIV-infected primary T-cells are concidered the natural "reservior" of HIV in vivo (Schnittman et al., 1989)
Thus, Gallo's controversial observation probably reflects the notorious difficulties experienced by his labratory in maintaining primary blood cells
alive in culture insted of a genuine cytociadal function of HIV (Crewdson, 1989; Culliton, 1990 Rubinstien, 1990, Hamilton, 1991).
Gallo showed in a later study from his labratory that about 50% of the uninfected T-cells died within twelve days in culture (Gallo, 1990). Indeed the
assumption that HIV is cytocidal is incompatable with generic properties of retroviruses and with specific properties of HIV:
1.) The hallmark of retrovirus replication is to convert the viral RNA into DNA and to deliberately intergrate this DNA as a parasitic gene into the
cellular DNA (Weiss et al., 1985). This process of integration depends on mitosis to succeed, rather than on cell death (Rubin and Temin, 1958;
Duesberg, 1989c). The resulting genetic parasite can then be either active or passive just like other cellular genes (Duesberg, 1987). Transcription
of viral RNA from chromosomally integrated proviral DNA also works only if the T-cell survives infection, because dying cells are not
transcriptionally active. Thus, this strategy of replication depends entirely on the survivival of the infected cell (Duesberg, 1987)
Noncytocidal replication is the reason that retroviruses were all concidered potential carcinogens before AIDS (Weiss et al.,1985; Duesberg, 1987)
Alternatively, it has been proposed that HIV protiens are directly toxic because of stuctural similarites with scorpion and snake poisons (Gallo,
1991; Garry et al., 1991, Garry and Koch, 1992). However, no such toxicity is observed in millions of asymptomatic HIV carriers, and there is no
reason why it should occur, if it did, only after latent periods of ten years.
2.) The propagation of HIV in indefinitely growing T-cells for the "AIDS test" was patented by Gallo et al. in 1984 (Rubinstien, 1990) and was
confirmed by Montagnier (Lemaitre et al., 1990). It is totally incompatable with Gallo's claim HIV kills T-cells. Such HIV producing T-cells have been
growing in many labratories and companies since 1984 producing viruses at titers of up to 10-6 virus particals per. mL, which is many orders of
magnitude more than is observed in humans with or without AIDS (Duesberg, 1989c, 1991a).
In view of this, Gallo postulates that T-cell lines in culture have all aquired resistance to HIV killing (Gallo, 1991).
However there is no precedent for this ad hoc hypothesis, as no other cytocidal virus has ever been observed that is cytocidal in vivo and in primary
cells in vitro, but is noncytocidal in cell lines in culture. It is also implausable that a potentally life saving cellular mutation, such as
resistance to the hypothetical "AIDS virus," would be restricted just to cell lines in culture, particularly if these mutations occur so readily that
they are found in all T-cell lines. (Duesberg, 1991)
HIV, like all other retroviruses, does not specifically infect T-cells. It also infects monocytes, epithelial cells, glial cells, and macrophages,
ect., and none of these are killed by HIV (Levy, 1988; Duesberg, 1991a)
Most other retroviruses also infect T-cells, which is why so many of them are suspected "T-cell leukemia" viruses
(Weiss et al., 1985; Duesberg, 1987; Blattener, 1990). Thus the assumption that HIV causes AIDS by killing T-cells is not tenable (Duesberg 1991)
Anyone with any questions regarding whats above, please feel free to ask.
edit on 14-12-2010 by alpha68 because: (no reason