viruses, evolution, and net traffic

Leonard Pattenden ddlpatte at mailbox.uq.edu.au
Tue Oct 7 10:51:44 EST 1997


On 6 Oct 1997, Ed Rybicki wrote:

> Hey, some traffic!!  Wow!
> 
> Now seriously: Paul Keese (now of National Univ of Singapore) stood
> up at the last Int Soc Plant Mol Biol meeting in Singapore (21-27
> Sept) with a very interesting theory / proposition to account for
> why most plant viruses have ssRNA genomes (and mammals have all
> sorts).  He maintains (or so my understanding goes) that organisms
> tend to have the viruses that they have defence mechanisms for
> (presumably because otherwise they would be dead).  Thus bacteria
> have mainly dsDNA viruses as they have restriction systems; mammals 
> have all sorts as the selection is on the basis of the virion outer 
> surface (immune system) - and plants have ssRNA viruses because they 
> have evolved mechanisms like gene silencing to shut off excessive 
> production of mRNA.  Fungi have a prepondeance of dsRNA viruses 
> because they have learned to live with them (vertically transmitted, 
> etc.).  VERY interesting...
> 
> However, Thomas Hohn (who asked the question) and I independently 
> realised that precisely the opposite may be true: that what we see in 
> an organism is what it CANNOT handle; that is, that classes of 
> organisms may be "genetically immune" to classes of viruses, and what 
> we see in any organism as an infection is what the organism is 
> learning to handle.

My understanding of Viral evolution - as a protein chemist working in HIV
- is that viruses are escaped genes. Thus - for example - in many
retroviruses we see the aspartyl protease which cleaves the GAG-POL polyprotein
precursors could possibly have arisen from a monomeric cellular enzyme and
by a process of gene duplication, fusion and then selection, resemble the
smaller homodimeric protease we see today. The implication of my beliefs
to your suggestions, is that propensities for particular viral types must
reflect the availability of the machinery within the cell. Ie if a plant
cell can produce reverse transcriptase which could be incorporated
somehow into a virus, then the feasability of an RNA virus is
increased. Similarly if on infection, defense mechanisms exist for
stopping R.T. from occuring in the cell, the likeliness of an RNA virus
existing is decreased.

Any comments? 

Leonard Pattenden
3D Centre for Drug Design and Development
University of Queensland.







More information about the Virology mailing list