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The genetic stability of Ebola virus

anon anon at ahabs.wisc.edu
Mon Jul 31 18:16:40 EST 1995

In article <3vj140$i7b at news.orst.edu>, Steven Poet <poets at ccmail.orst.edu>

> Another possibility is that the reservoir species does not have a 
> mammalian immune system.  This Ebola strain, therefore, is capable
> of escaping into this reservoir and then emerge, unaltered, back into
> the human population.  Those PCR primers are most likely designed
> with a mammalian immune system bias.

Evolutionary pressure as a result of the host immune system, or other
antiviral defenses would affect the "transmission" of mutations that
altered the amino acid sequence of Ebola-encoded proteins.  That is
because these changes may bring about phenotypic changes (slower or faster
growth in a host, escape from immune surveilance, etc).

Mutations that don't change the primary structure of Ebola proteins
("silent" mutations, which can be found in coding or non-coding regions)
are not expected to be selected by Darwinian evolution  because they do
not result in phenotypical changes that can be selected (in most cases: 
With ssRNA viruses, silent mutations may affect the secondary structure or
the stability of the genome I guess). 

Why do we see so few _total_ (silent and non-silent) changes between in
Ebola 1995 and Ebola 1976...viruses separated in time and space.

I agree with Don Haut that the filovirus RNA-dependent RNA-polymerase must
be a very accurate enzyme because we see so few total mutations. 


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