Tom,
The link between HHV and KS is a relatively recent development, although
HHV had been suggested as possible co-factor in KS development in people
with AIDS. It wasn't considered an opportunistic infection since their
was no good evidence for a viral etiology. It simply appeared to be a
malignancy strongly associated with the peculiar type of
immunosuppression seen in AIDS. KS, as you know, is not a new disease.
Rather, the disease had previously only been seen in heterosexuals with
immunosuppression from other factors, ranging from old age to transplant
and cancer therapy.
The back and forth between different groups of researchers is, as anyone
familiar with science knows, normal scientific discourse. This is part
of how the work gets done. To prestigious groups of scientists make
their statements based on their own observations, and then set out to
prove their case as convinvingly as possible.
I don't know why you mention CFS, but since you brought it up, their
isn't a shred of conving evidence that CFS is associated with any known
virus. The spread of different herpesviruses depends on the virus. Not
surprising. Varicella is respiratory, EBV is saliva, HSV by saliva and
sexual contact. So what?
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.
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 want an example of how this
could happen?
A recent report in Science showed that another herpesvirus, this time
CMV, encodes a homolog of one of the secondary receptors for HIV entry
into cells. In vitro infection with this herpesvirus allowed HIV to
infect cells which were previously resistant because the cells now
expressed the needed receptor. One virus helps the other. Now take it a
step further and say the second virus suppresses immunity, allowing the
first virus to become pathogenic and cause cancer, perhaps.
Jay Mone'
