> "the probable evolutionary history back several hundred milion years."
Only for geminiviruses and potyvirses, and Adrian Gibbs et al. mostly did it for
> As I see it, trees have two separable uses. For one they can be
> used for taxonomic purposes, for saying which viruses are most closely
> related to one another and how closely related groups of viruses are to
> one another.
> less sure. In some cases (cases where there are lots of OTU's to look
> at), the data are consistent with a star topology, everything radiating
> from one common ancestor sequence.
This happens with generic potyviruses: apart from a couple of
recognisably distinct subgroups (eg: viruses related to BCMV, viruses
related to BYMV), the viruses appear to "burst" from a common source
- but are all more related to one another than any are to generic
bymoviruses or rymoviruses, implying an ancient sepration between the
three genera before "speciation" of generic potyviruses.
One interpretation of the star
> topology is that there are only certain sequence classes in sequence
> space that are consistent with a successful infectious virus. If
> viruses evolve, they jump from one of these "fitness" peaks to another.
This is an intriguing concept: it could explain the apparently
discontinuous distribution of sequence variation with the Potyviridae
and Geminiviridae, where strains and species appear to have a
foundation in discrete ranges of sequence variation ("mountains" in a
plateau of variation, when percent sequence difference is plotted
against incidence of variation for all pairwise comparison of 40+
> Here is my concern. If we have a tree whose statistics suggest
> that the star topology is not applicable, how can we be sure that the
> topology implying a line of descent is not due to limited sampling? If
> we gather more and more sequences of related viruses, might we not find
> that our initial tree was erroneous and we are really dealing with a
> star topology?
Surely this can only be answered by collection and analysis?
> HIV-1 studies come to mind here. ... Is it possible that there are only a limited
> number of regions of sequence space (corresponding to subtypes)
> compatible with a successful HIV-1? This would mean that the sequence
> space between subtypes consists of HIV-1's with poor "fitness". It
> would also mean that the subtypes were generated by rare events of a
> virus of one subtype jumping into another peak in sequence space.
> Arguing against this are the observations of apparently successful
> recombinants between subtypes.
HIV I believe is a special case: a retrovirus with an abnormally high
mutation rate (even compared to other retroviruses) can not be held
up as a model of anything except accelerated evolution n action, or
of an emerging pathogen coming to terms with a new host system. Even
the RNA potyviruses - which one might expect to have a fast rate of
evolutionary change - appear to be traceable in terms of evolution,
to a far greater extent than HIV. Perhaps because there is far less
selection going on in that plants don't have equivalent immune
systems. Perhaps the same goes for Ebola...
> I feel that I am at the limit of my knowledge and understanding.
> Thus, I stop and would appreciate reading corrections and other
And so would I! I work in too much of a vacuum; I would appreciate
constructive comments on some of these phenomena/ideas.
| Ed Rybicki, PhD | ed at molbiol.uct.ac.za |
| Dept Microbiology | University of Cape Town |
| Private Bag, Rondebosch | 7700, South Africa |
| fax: x27-21-650 4023 | phone: x27-21-650-3265 |
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"And then one day you find, ten years have got behind you"