Jay,
>> It shouldn't be surprising that you see differences in the pathogenesis
> of a virus in different populations. Consider EBV. In North America,
> the primary disease caused by this herpesvirus is infectious
> mononucleosis. In African children, a major manifestation of EBV
> infection is Burkitt's lymphoma. While in mainland China, you see
> nasopharygeal carcinoma. Same virus, three very different outcomes.
> Why? Hard to say, but probably some combination of genetic and
> environmental factors. In addition, these factors would be different for
> other viruses which display the same types of differences.
Thanks for your comments.
I imagine that many of the heterosexual AIDS victims in the U.S. are
black, who would have little genetic difference from black Africans.
Neither would there be genetic differences between white gays
and white heterosexuals in the U.S.
Environmental differences? Of course- I'm suggesting some:
poppers, lubricants. We can imagine others, but we have to identify
them and make a case for them.
> Today, KS is seen predominantly in gay men. Precisely the same
> population that is predisposed to HIV. Not surprising since one
> infection may predispose you to another
You seem to be using the logic:
* gay men get more HIV
* HIV indirectly leads to KS
Therefore: gay men get more KS.
The problem is, this logic isn't quite adequate. Yes, gay men
should get more KS than the GENERAL population. However, the percent
of HIV+ gays who get KS should not be different than the percent of
HIV+ straights who get KS - UNLESS we come up with some other factor
to explain why HIV+ gays should have more HHV8 (or whatever cofactor),
than do HIV+ straights.
We cannot rely simply of convenient stereotypes of "promiscuous gays"
as the excuse why we might suppose that gays would have more HHV8.
We are comparing to straights who are specifically HIV+, so it is reasonable
to imagine that this group would also be quite sexually active.
Herpes is hardly an uncommon infection among straights. This doesn't
mean the KS-causing variants are NECESSARILY similar in this regard,
but it would not be unreasonable to postulate that it would be little
different,
until we have any better evidence.
If you compare the gay/straight herpes infection ratio among sexually
active populations (again, not merely the general populations), I would
wager that
it is insufficient to support the degree of difference in the KS ratios
that we see.
Anyone care to present data? (I will also be looking for it).
