Just wanted to pick at a few things that were posted recently by Jeff
regarding virus evolution.
>Viral evolution is dependent random genetic drift.
...is what "dependent random"...an oxymoron???
>a virus does not benefit by completely killing its
>host--unless it can transfer rapidly from host to host.
>This transfer is more productive if it is laterally (to a new host) than
>serially (to the same host).
Huh?? Guess my misunderstanding of this statement is how you are defining
the spread - I've heard of vertical and horizontal transmission but never
serial and lateral in the context you are presenting it.
>Since viruses replicate at very high numbers within their host, they can
incur >significant mutations,
Ummm....not really. Is the viral genome DNA or RNA, what is the fidelity
of polymerase(s) (viral or host) used in the virus replication, is it a
DNA virus which replicates through an RNA intermediate (retro and
pararetro), etc. And what is defined as "significant"? 10%? 50%? What
level of variation from "wild-type" constitutes significance?
>partly due to the streamlined genome;
Streamlined???? Try telling that to someone studying herpesviruses or
vaccinia to name just two ;-)
>these mutations are random--natural selection then acts upon a randomly
mutated >population of viruses.
Careful. Selection, definitely; natural, not always. Antiviral agents,
like AZT and 3-thiacytidine, are chemically synthesized and not found in
nature; resistance to these agents *is* seen in HIV-1.
Well...enough blathering. Cheers and a Happy St. Patrick's Day.
kfischer at gpu.srv.ualberta.catyr-2 at bones.biochem.ualberta.ca