a molecular evolution question re ebola

[bhjelle at unm.edu]

In article <3pu9ke$59f at agate.berkeley.edu>,
 <salamon at allele5.berkeley.edu> wrote:
>
>
>Has anyone access to the molecular data that led to reports that
>this latest Ebola zaire outbreak is due to virus little changed over
>the past 20 years?
>
>I'd like to see that data.

I suspect it will be published some day ;-).


>Where could this virus have been where it did not experience
>much genetic drift?  Any ideas?


This question reflects a misconception about the stability
of the genomes of RNA viruses in nature. Given a host in
which the virus is comfortable, whether that be monkeys,
rodents, or plants, genetic drift is really minimal. In
our own experience with Four Corners hantavirus, for
example (another minus-sense RNA virus), sequences separated
by 20 years differ by only 2% at the nucleotide level, and
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.


>Does Ebola (or do filoviruses in general) use reverse trascriptase?
>Can it exist as a provirus?  That could slow the accumulation
>of substitutions.  But something tells me I've heard it doesn't
>integrate itself into host DNA.
>
No there is no RT. The degree of adaptation between a virus/host
unit is more important than the use of a proviral intermediate
in determining a virus' genomic stability. Thus, HIV is mutating
rapidly as it passes through humans, but HTLV-I evolves at
a snail's pace. Both use RT and proviral intermediates.

Brian