1918 influenza evolution

Giovanni Maga maga at vetbio.unizh.ch
Thu Mar 23 08:03:35 EST 1995


In article <Pine.SOL.3.91.950321170508.15087A-100000 at corona>, Patrick
O'Neil <patrick at corona> wrote:

> From bhjelle at unm.eduTue Mar 21 16:28:25 1995
> Date: 20 MAR 1995 06:56:22 -0700 
> From: bhjelle at unm.edu
> Newsgroups: bionet.virology
> Subject: Re: HIV-1 vs HIV-2 
> 
> >
> >>Not necessarily.  The flu pandemic of 1918 is a nice case in which a
> >>previously standard flu strain in the United States quickly evolved into a
> >>major killer in the trenches of late World War I. (...del...)

Well, in the case of flu, the high mortality can be also ascribed to the
superinfection with bacterial pathogens (f.e. S. aureus) in the respiratory
tract, which find more favourable conditions due to the damage of the
epithelium by the virus. Since in 1918 there were almost no valid
antibiotics available, I think that fact played a main role. In addition
the enviromental conditions were critical (as you pointed already pointed
out), so the final result was a combination of mutations in the viral
strain plus other factors virus-independent. 

That
> is why I tie the two concepts together in this circumstance:  easy
> transmissibility and selection in favor of high virulence.  
> 
> Patrick

Again, I do not see where is the *selection* in favour of high virulence.
You just said that there was *no selection* against them. You said that
under the circumstances described there was no need for the virus to be
slow. But, at the beginning was the virus slow or fast (in term of
replication and spreading)? If it was slow, then your argument should
better say: there was anything against the mutation from slow to fast, but,
being the soldiers so closed to each other, both fast and slow viruses
could spread as well. It is possible, of course, that the final result is a
homogeneous fast population (since the more progeny you spread, the more
your genotype is fixed in the population) if they kill the host before the
slow variant can reproduce and the host number is reduced such that 100%
are infected by the fast variant. But since the mutation rate at each
generation is high, the frequency of the *fast genes* transmitted to a new
generation against the frequency of *slow genes* could attain a substantial
equlibrium, due to back-mutations from fast to slow. I also think that rate
of transmission from host to host and rate of replication within the host
must be considered separately. They are also under different genetic
controls.
Would like to hear your opinion, anyway, since I got that you work on viral
mutability.
maga at vetbio.unizh.ch



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