The Kaposi's Sarcoma Enigma

Jay and Nancy Mone jaymone at PAONLINE.COM
Sat Sep 4 07:38:25 EST 1999


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'



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