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HIV-1 vs HIV-2

bhjelle at unm.edu bhjelle at unm.edu
Thu Mar 16 13:22:08 EST 1995

In article <Pine.SOL.3.91.950315150526.11901A-100000 at corona>,
Patrick O'Neil  <patrick at corona> wrote:
>> > The most parsimonious scenario of all has an HIV ancestor 
>> incubating > within human populations for about a thousand years or 
>> so, with jumps > into various simian lines within the last few 
>> centuries.
>> Whaaaaaaaat?  Says who?!  All of a sudden, HIV has been in HUMANS 
>> for a thousand odd years, and gets BACK into simians??
I too have not heard of this scenario. The first thing to do
to straighten this out is to make it clear whether you are
talking about HIV-1 or HIV-2. They probably have totally
different evolutionary histories, at least in humans. Molecular
clock estimates for divergence of HIV-1 from HIV-2 (or SIVs)
generally converge somewhere in the neighborhood of the
last few decades, not thousands of years.
By contrast, some SIVs are essentially identical to some HIV-2s,
and transmission of SIV into man has been observed in
real time, in a primate colony worker. It is probably
legit to call that virus an HIV-2, though I don't think
anyone has done so.

>As for a century or more period of time evolving in humans, this is not a 
>big problem either.  If it started out rare and rather benign as is the 
>case with most retroviruses, then it could lay about for any period of 
>time until some series of mutations and selective pressures began to 
>favor a more pathological form (high sexual intercourse rates within and 
>between populations is certainly going to favor higher pathogenicity.  
There seems to be some confusion here between high transmissability
and high pathogenicity, which are totally different things.
I don't know how one can conclude how retroviruses "start out"
in natural situations, but when SIV is introduced into a non-
native host, like a macaque, it starts out as an explosively
pathogenic virus.

>Low pathogenicity within a host doesn't necessarily a "better" adaption. 
>If selective pressures within a natural host population favor rapid
>transmission and pathogenesis, then it will develop in that direction
>regardless of how long the virus has been floating around within the host

For a virus that has historically probably been spread sexually
(such as lentiviruses) it seems clear that high, acute pathogenicity
will not favor transmission. Airborne or fomite-borne viruses
are another matter.

>Low pathogenicity within the host might just as well indicate a recent 
>move into that population, meaning that the virus hasn't quite developed 
>for maximum efficiency within that host, just as an overly high 
>pathogenicity could mean the same thing IF it reduces the rate of 
>successful transmission.

For viruses, as opposed to certain parasites, there is quite
a bit of support for the notion of adaptation toward low
pathogenicity for the native host, while having significant
pathogenicity for non-native hosts.ri. 


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