Virus variation

[Lyle Najita]

In article <3a0ndlINNami at early-bird.think.com>,
york at mbcrr.dfci.harvard.edu (Ian A. York) wrote:

> In article <9411111848.AA02302 at ariel.med.pitt.edu> bap at MED.PITT.EDU
(Bruce Phillips) writes:
> 
> [mutation rate in HIV, possible role in immune evasion . . . ]
> 
> >     I did not mean to imply that recombination does not play a
> >significant role in generating diversity in influenza viruses- but
> >it does not seem to play a role in any given virus's ability to
> >escape immune response ONCE INFECTION OCCURS.  Without question,
> >genetic shift accounts for the appearance of flu viruses for which
> >pre-existing immunity (or cross-immunity) doesn't exist.
> > 
> 
> This is a very interesting subject, I think.  To extend the discussion to
> other lentiviruses, I recall that Maedi-Visna also shows variation in
> infected hosts.  I also recall (though this is foggy) that the mutations
> appeared to follow a semi-regular pattern - almost as if there was a
> program for mutation use.  (I think that the much more complex protozoal 
> parasites may do the same thing; completely off topic, I guess.)  One 
> would expect this to be of use only in persistent viruses and especially 
> in viruses which continue replication within the host (therefore ruling 
> out, for example, herpes simplex virus).[stuff deleted]

I don't mean to nitpick, but isn't a cold sore flare up an indication of a
burst of HSV replication?

To get back on track and to get a burning question answered, does anyone
know why vaccination is not performed with a recombinant flu vaccine
bearing all major hemagglutinin and neuraminidase types (ie - H1, H2, H3,
etc.) instead of the best guess as to what will be prevalent for the
coming "flu season"?

Lyle