In article <3009bb616c55002 at gold.tc.umn.edu> "Jeffrey John" <john0390 at gold.tc.umn.edu> writes:
>have.The herpes virus I work with is a herpes viru(Lucke Tumor Herpesvirus) that
>infects north americam leopard frogs.It was the first cancer to be associated
>with a herpes virus and confirmed using Koch postulate
Are you sure about this? I had thought that Marek's disease (of chickens)
was the first tumour to be associated with a herpesvirus; and also,
incidentally, the first tumour for which a vaccine is available.
>I would like any of your in put as to how you think the genome of the herpes
>virus plays its role in causing the infected cells to poliferate uncontolablly
>and thus become carcinogentic.
There are several other herpesviruses which are associated with tumours,
and it seems likely that they use different mechanisms of oncogenesis. I
don't think any are very well understood. Epstein-Barr virus, of course,
is the best example in humans. There are quite a few reviews and papers
on this. Herpes simplex virus, particularly type 2, has also been linked
to cancer. The linkage is mostly epidemiological (in that people infected
with HSV2 are more likely to get cervical cancer; the risk ratio is
unspectacular but is moderately convincing, I think. Not all studies find
such an association). HSV2 also can cause transformation of cells in
vitro at low frequency. In this case it seems to use a 'hit-and-run'
mechanism, in that the transformed cells don't maintain any herpes
sequences. Mechanism is unknown. The 'hit-and-run' hypothesis is being
suggested for the putative Kaposi's Sarcoma Herpes Virus as well, in that
despite the recent epidemiological links between KSHV and some forms of
KS, KS cell lines in vitro apparently don't have the KSHV genome
detectable. This is all quite controversial right now, I think.
In sum, different herpes viruses appear to use different mechanisms, and
these mechanisms are poorly understood. I could speculate, but I don't
think there's enough known for these speculations to be more than general
statements of principal.
There are some fairly obvious starting points for your project, I think,
and I assume that at least some have been done or are under way (does the
viral genome stick around? All of it, or just part? And other fairly
classical tricks and approaches.)
Ian York (york at mbcrr.harvard.edu)
Dana-Farber Cancer Institute, 44 Binney St., Boston MA 02115
Phone (617)-632-3921 Fax (617)-632-2627