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Re: vinmantoo post# 117922

Friday, 04/08/2011 3:26:02 PM

Friday, April 08, 2011 3:26:02 PM

Post# of 253608

Hepatitis C has only a single RNA molecule for its genome, so it requires a template switching event. This means it is quite different and limited in both the probability and the range of phenotypic variation that can arise from any putative recombination event as compared to influenza.



I am not knowledgeable about the detailed mechanics of different viral-types' replication, but:

a) There is data to indicate that HCV recombo does happen across different strains. See link at bottom, among others.

b) And recombo probably happens orders of magnitude more commonly when it is all the same sub-strain within the same human. (as per link at bottom, HCV is fragile wrt to recombo across strains - but the closer the strains the better it does).


In any event, the error prone nature of the vial replication via RNA dependent RNA polymerase will generate far more variation than any template switching.



1) Variation is just one part of evolution (I am not trying to start a semantics debate - filtering (i.e. selection pressure) and recombo are the other two parts).

2) In an adequately variant population breeding (aka recombo) is a very(!!!!) powerful evolutionary tool when having to make rapid change to accomodate two (or more) simultaneous or almost simultaneous threats to existance.


Cites:

See section on 'recombination':

http://vir.sgmjournals.org/cgi/content/full/85/11/3173
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