From: quilty@PHILOS.umass.edu (Lulu of the lotus-eaters)
Subject: HIV/AIDS Link -- followup inquiry
Note: Copyright 1992, Dan R. Greening. Non-commercial reproduction allowed.
Archive-Number: 33
Organization: University of Massachusetts, Amherst
Date: 25 Jan 1993 18:39:06 -0500

     I posted an inquiry to this group recently, requesting
information on the doubts Duesberg and others have expressed about
the alleged link between HIV and AIDS, and the effect upon this
doubt of recent evidence of higher rates of T4 cell infection.  In
a responding post, Matthew P Wiener, has largely denounced
Duesberg's scepticism; and by extention, I believe, my question.
I would like to provide some excerpts from a fruitful email
conversation I have had, which clarifies the reasons for my doubts
about the HIV/AIDS link.

     As before, I would be extremely interested in hearing from
anyone with further information on this question.  As I mentioned
before, I am not a biologist or virologist; however, I am an
intelligent enough layperson to wade through technical papers if
someone sends me them.

   .....[My Correspondent].....
   I don't have any info on what Duesberg and others have to say, but I can
   say something about the issue of HIV infecting cells. Viruses work by
   insinuating thier DNA into the DNA of the host. Some viruses can stay
   dormant for years, only later to have an effect. In fact, there is evidence
   that there are provirus sequences (sequences of viral DNA) that have been
   passed down to us over many many generations. Think about it, if 20-30%
   (high estimate) of T4 cells are infected, and once in a while, a few  of
   these become active and start replicating HIV, you can see how you might
   see a slow decrease over time in T4 cell count.

.....[Myself].....
Thank you for your above response.  I think, however, that it
fails fully to appreciate the significance of the chemical
inactivity of HIV in human T4 cells.  I understand that viri can
remain dormant in cells for many years, or even cross-
generationally; such seems clearly to be the case with HIV.
However, a "normal" virus must regain its chemical activity before
it can have a renewed effect on a host.  Even if they had "done
nothing" for years, viri can restart their host-cell's active
reproduction of viral clones, and hence have a negative effect
upon their cellular host.  But "normally" they do this by becoming
active in a significant percentage of host cells.  However, this
is not the case for HIV.  Even if it infects 90% of T4 cells, it
remains latent in all but .01% of these cells at any given time.
This latency is not *even*, but *especially* during the late
stages of AIDS.  That is, those most accutely suffering from AIDS
often have the lowest rate of cellular HIV replication.  You are
quite correct about HIV becoming "once in a while" active, but
this "once in a while" is (as I mentioned) such as only to affect
approx. 10^(-4) T4 cells.  Even if HIV were to kill every cell
actively involved in its replication, the rate of depletion of T4
counts would be substantially lower than their rate of
replenishment (even at the lowered replenishment rate of AIDS
sufferers).

   .....[My Correspondent].....
   Good point. Where does the .01% figure come from? Does that vary with
   individuals and over time? And what is the replenishment rate for T4 cells?
   I'll admit to not being either a virologist or an immunologist, but I am a
   biologist, and it seems that there is more information needed to really
   figure this out. Also, I thought that the reason that people in the late
   stages of HIV disease had the lowest HIV replication rates was because of
   the small pool of cells available to replicate in.

.....[Myself].....
     The figure of 10^(-4) is of course an approximation which
varies between individuals and over time; but I've generally seen
it presented as the UPPER end of a plausible range.
     I read the figure in two Duesberg articles, one in _Cancer
Research_, the other in _New Englang Journal of Medicine_.  I'm
sorry I don't have exact cites for either, but a quick trip to the
citation index by author will find them.  The first was
early, like maybe 1987, and was one of the first pieces to
question the HIV/AIDS hypothesis in a major scientific journal.
The other was a couple years later, though it is also a couple
years ago now.  I've also seen secondary or tertiary articles on
this area in the popular press (_Spin_ magazine does a
particularly good job with this).  The original 10^(-4)
infection/replication rate was actually done by researchers under
Gallo (who was listed as joint author).  Gallo, however (fraud
that he is), has tried vehemently to deny the consequences, and
even factualness, of his own findings.  Some further research has
managed to find rates as high as 10^(-3) in individual cases, but
these would be exceptionally high, and are not necessarily (and
more likely *NOT*) in those acutely suffering from AIDS.
     I don't know exactly what the replenishment rate of T4 cells
is, nor even the exact units in which such a thing would be
expressed.  But what I've heard is that, normally, it takes about
a month completely to replace the T-cells (of all categories) in
your body.  It's difficult to make this exactly commensurate with
a given rate of HIV replicating cells.  What comparing these
things basically depends upon is an estimate of how *quickly* HIV
replication could conceivably kill a host cell.  The problem is
that *IN VITRO*, at least, HIV replication *hardly ever* kills
host cells:  that is, cellular cultures which are induced or
selected for HIV replication survive *indefinitely*.  Even the
speculation of those whom I've seen mentioned in the popular press
who are most dogmatically pro-HIV/AIDS link, only suggest that HIV
replication might kill a cell *in vivo" in the course of *DAYS*.
Even assuming a kill time of *ONE* day, and a replication rate of
10^(-3) host cells, this only gives us 30 x 10^(-3) = 1/30 of the
cells killed during their month-long replication cycle! And these
are outside assumptions on everything favoring an HIV explanation.
     The long and short of it is the the HIV/AIDS explanation has
a *BIG* conceptual gap in the middle of it.  I won't dogmatically
conclude that this gap can't be filled; but neither will I
dogmatically believe the hypothesis based simply on the word of a
medical-research establishment deeply intermeshed with political
biases, and a standard of truth subsumed to personal power games
(by Gallo, particularly -- but others also).

   Also, I thought that the reason that people in the late
   stages of HIV disease had the lowest HIV replication rates was because of
            ^^^^^^^^^^^
   the small pool of cells available to replicate in.

If you mean "replication rate" as a total rate of HIV production,
this is true, though somewhat irrelevant.  If you mean
"replication rate" as a percentage of T4 cells active in the
replication process, then this is pointedly not true of people in
late-stage AIDS (who usually have lower such rates than people
during early, asymptomatic infection).  Btw.  I don't know what
"HIV disease" is! I can only talk about AIDS, since I believe that
HIV infection is generally benevolent and asymptomatic (except
mild flu-like symptoms *immediately* after infection).

yours, Lulu...

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