On Sun, 16 Jan 2000 CurtAdams@aol.com wrote:
> In a message dated 1/15/00 22:31:22, Doug Jones wrote:
> >"Eliezer S. Yudkowsky" cited:
> >> > The drug fits neatly into a groove on the
> >> > surface of the virus, gumming up the machinery it needs to infect the
> >> > body's cells.
> >But isn't the coat protein of the common cold very mutable?
> >Pleconaril-resistant strains will arise very quickly, and back to square
> The highly mutable outer coats proteins shield less-mutable receptors
> from immune surveilance. The receptor would be much harder to
> mutate and still preserve function. I assume that's the target.
> There may also be conserved regions in the coat proteins as well.
Actually cold viruses (rhinovirus) are pretty "immutable".
The problem is there are about 70 different strains, so
you can catch 1 cold a year for your entire life. After
you catch one strain, you are relatively immune to it until
your immune system starts to get weak (in the elderly or
immunocompromised). The other major nasty virus is influenza
because it is a multi-"chromosome" virus and the human and
animal strains can recombine in multiply infected individuals
to produce a new variant every year. Most other viruses have
fewer strains and don't mutate very fast (with the exception of
You have to read the fine print in the press releases. It would
appear that they are going after a *generic* mechanism in the
process of the viruses "decloaking", thats why it is effective
in multiple types of viruses.
If anyone sees anything specific on the exact point of interference,
please email me because this sounds like an insight into viral
processes which was unknown during my education.
This archive was generated by hypermail 2b29 : Thu Jul 27 2000 - 14:02:20 MDT