a molecular evolution question re ebola

bhjelle at unm.edu wrote:
: only 1% at the amino acid level. Even those differences
: are quite possibly a consequence of sampling different
: lineages, not a genuine measure of the rate of evolutionary
: change over time.

: All of the talk about the inherent poor fidelity of RNA-
: dependent RNA polymerases (1 in 10-3 - 10-4 misincorporation
: is typical) is true, but in nature we are measuring
: *predominant* species of viruses, in settings in which the
: viruses rarely encounter a genetic bottleneck that might
: favor significant genetic drift. In the absence of such
: bottlenecks, it is unlikely that RNA quasispecies will
: change en masse. Only nonsynonymous changes are likely
: to undergo substantial selection, and, in a longstanding
: virus/host relationship, the vast majority of such changes
: are deleterious to the virus.

Intersting.  So, which is nearer to what you are suggesting:

The sampling effects on a virus are minimal because

	a) there are many hosts at one time
	b) a fair sized population of virus particles enters each new
	host, and evolves little in a host (not true for HIV)

A large population of virus (what is an individual? one particle?
all the virus in one host?) should be less subject drift, but
should evolve more subtle adaptations.  I am having difficulty
accepting that viruses do not experience population bottlenecks.
An outbreak can be due to a single infected individual.  Say the virus
then returns to a more endemic state somewhere.  Such a mechanism would
provide ample opportunity for sampling effects.  My question
relates to where it resides such that it does not experience sampling
effects.  I do understand that you are suggesting it is quite
normal for there to be a sufficient population (and mixing among
potential host) that a predominant strain lasts a long time.
Surely new varieties arise either through strong advantage or
through some sort of "allopatric" diversification.

I am wondering why HIV is so diverse (and resides succesfully entirely in
human populations) while Ebola Zaire (we have had suggested) is
relatively static (appearing sporadically).  Does the answer lie in different
molecular/physiologcal mechanisms, or in different population dynamics?
If it is the latter, it suggests to me that E. Zaire normally resides
in a large population of extremely well mixed host (over the time of
several virus "generations").

Just trying some thought experiments.

Hugh

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