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RNA pol, replication fidelity

ijiwaru at wheel.dcn.davis.ca.us ijiwaru at wheel.dcn.davis.ca.us
Fri Dec 1 13:47:17 EST 1995

In article <49lpml$s76 at daily-planet.nodak.edu>,
schoffma at badlands.nodak.edu (Scott A Hoffman) wrote:

> Question for anyone.   
> Recently, I've attended a few seminars on viral pathogenesis.  An 
> interesting topic that seemed to crop up from time to time was that a few 
> RNA viruses (most notably Ebola and Dengue) show a high replication 
> fidelity.  This is interesting since to my understanding RNA viruses tend 
> toward high rates of mutation, the idea is that the replicative machinery 
> is inefficient.  The question of course is why?  Why, should one virus 
> show high rates of mutation and others not.  Is there any evidence that 
> the replicative machinery (RNA pol, etc.)  of some viruses are more 
> efficient.  Is there something inherent in the secondary structure of 
> some viruses that may lead to lowered mutation rates.  To what degree 
> does natural selection play a role?  I could envision a situtation in 
> which a number of progeny are made (the replicative machinery is just as 
> inefficient as other viruses) but the conditions are so stringent for 
> survival that only those sequences that show a few base pair changes can 
> still be viable.  This however begs certain other questions.  For 
> example, as I understand it, Dengue reaches high virus titers.  As it 
> turns out, each virus is as viable as the next, and for good reason:  The 
> mosquito vector requires high virus titers to become infected.  No 
> vector infection - no transmission.  It seems counterintuitive that 
> selective pressures play a huge role, if they did then one would expect 
> lower virus titers (unless of course, that virus replication continues 
> at very high speeds).  Well, I feel as if I'm beginning to babble. So 
> I'll leave the question open.   Does anyone have any ideas, thoughts or
>  information?  Do I even have all the facts straight?    Thanks.
> Scott Hoffman
> Graduate Student
> schoffma at badlands.nodak.edu

There is much evidence that supports the idea that the error rate of RNA
polymerases is much higher than the error rate for DNA polymerases.  For
that very reason it has been suggested by numerous researchers that we not
consider RNA viruses as homogenous genetic entities but rather as
quasi-species.  Then upon a change of host or host environment, one would
be able to observe the appearance of the most suitable dominant genome for
that environment.  The mutated genomes are still present in any given
population, when we sequence these genomes, we are looking at the
"consensus" sequence at any given position.  High apparent fidelity of
replication, or the lack of mutations, may indicate a rather strict
requirement for specific sequences.  This could be caused by the virus
having intricate regulatory requirements, the need to have conserved
protein function (you wouldn't want to interrupt the polyprotein before
the full-length has been translated) or structure (certain conformations
required for proper processing), or the need for conserved nucleic acid
secondary and/or tertiary structure (as you have already alluded to). 
Keep in mind, that if the virus is very efficient at replicating its
genome, you may not necessarily detect a lag caused by having a minor
subpopulation of viral genomes taking over the host from a previously
dominant viral genome.  I hope someone else will pick up this thread
before it breaks down to all the "it was made in a laboratory" psychos.

Lyle Najita
Plant Pathology
University of California - Davis

My opinions are given freely.  As such they are worth exactly what you
paid for them.

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