Christopher please read this

David Peritt Peritt_d at
Wed Apr 5 09:44:24 EST 1995

In article <3lqq8b$mef at> Christopher Savoie,
savoie at writes:

>> There is no evidence that I know of showing direct CD8 infectivity.  
>> CD4+8+ thymocytes can be infected but once they become single positive
>> they are presumably resistant.
>Excuse me, but please take your premise to its logical conclusion. If
>the double positives are infected (they are), then they will never 
>become fully functional single positive CD8's in the first place.
DPs are infected but not 100% of them.  There is a normal number of CD8
in the periphery.

>> The affect of HIV on CD8 cells and vice versa is heavily studied and
>> important.
>Actually, I have seen many studies on the _role_ of CD8's in HIV
>and the changing efficacy against certain HIV class I epitopes over
>time in carriers, but nothing much that lends an explainationto
>the eventual  demise of class I restricted immunity at the end 
>stage of infection.  And nothing that explains how the infected 
>precursers are cleared.  
the literature is full of studies looking at the many ways CD8 may be
involved in HIV clearance.  Some of them not related to the classical
class I killing of infected cells.  Remember that CD8 probably need CD4
for optimal function.  so when CD4 is dysfunctional so are the CD8.  The
putative mechns are discussed in the literature.

>> They do not drop dead at all.  In fact there are relatively normal
>> of CD8 but they may not be functioning properly and this is being
>> investigated with ernest.  Jay Levy's story for instance is
>Tell that to AIDS patients with runaway EBV lymphomas that are
>very easily controlled when one has a nice set of functional
>CD8 effectors. 

I will say it again.  There are normal levels of CD8 cells but they may
not be functioning properly. they may not be functioning properly. they
may not be functioning properly. they may not be functioning properly.
they may not be functioning properly. they may not be functioning
properly. they may not be functioning properly. 

You should read the post you are responding to.

>CD8's are definately impaired by HIV 


>and probably because the precurser population eventually runs out.  

huh??  We just said that the levels of CE8 are nearnormal until death of
these patients.  The infectivity of the precursor decreasing CD8 cells as
a mechanism can not be true.  That precurser population IS INFECTED, so
why is it necessary
>to argue otherwise?  Their overall levels may be "normal" until
>the end, but high CD8 counts are a  given during clonal proliferation
>against a viral infection.  
I am lost.  There is a normal number of CD8 cells.  You blame this on
clonal expansion.  This may be true.  But that is a normal level of CD8
cells.  Homeostasis keeps the level realtively constant.  The body
therefore does not make new CD8 cells.  Is this what bothers you?  This
is interesting but completely unrelated to the infection of the DP cells. 
>Anyways, how does Levy contradict what I say about a CD4CD8 dp precurser
>population being a prime target for HIV infection and hence
>CD8 dysfunction/death?
Jays data is just one example of how CD8 dysfunction and function are
being studied.  I mention it because in your post you went on about CD8
and CD4 studies were not interacting which I strongly disagree and gave
this example.

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