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HIV-1 vs HIV-2

bhjelle at unm.edu bhjelle at unm.edu
Mon Mar 20 08:56:22 EST 1995


>
>>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.  The flu is easily
>>transmissible as it is but get a handful of sick soldiers in a crowded
>>trench where even if they are incapacitated by illness or combat injury
>>they can STILL easily transmit to others, and you have the evolutionary
>>pressure to select for particularly deadly and quick acting variants.  The

>Again, I don't understand the firm connection in your mind between
>transmissability and virulence. These concepts should be dissociated.
>Clearly the ease of transmission affects a the ecologic
>success of viruses, but the role of virulence is less clearcut.
>Does a dying soldier transmit influenza virus more effectively than one
>who is destined to survive?

In this circumstance, the sick soldier is not going to be isolated from
the other soldiers to prevent spread and allow recovery.  The unfortunate
soldiers, therefore, easily transmit virus to fellow soldiers who will
also not be isolated.  Since so many hosts are so easily available and
there is no need for slow incubation or viremia development -- the virus
doesn't need to reproduce slowly in order to insure that a STILL mobile
host can encounter other hosts and pass on progeny.  The sick soldier,
just laying there coughing and sneezing, is very capable of passing on
virus to neighbors who will easily pass it on to others, etc.  In this
case, the fastest, most virulent variants have the upper hand over low
virulence variants, unlike normally, and even as they quickly lay up the
host, the host is still effective in passing virus on to new host.  That
is why I tie the two concepts together in this circumstance:  easy
transmissibility and selection in favor of high virulence.  Under normal
circumstances, a victim of flu is available to transmit virus to new hosts
only for a day or so before calling in sick.  Barring that, our workplaces
and homes are not anywhere near as crowded as the trenches were so that
even if a flu victim continues working and/ or fully interacting with
family members, the host population is not as dense and, therefore, not as
accessible.  Less virulent variants are the only ones that succeed in
being passed on -- the more virulent variants lead to the host being
isolated (in a hospital or in their beds) and potential new hosts become
few and far between. This is the antithesis of the circimstances of the
WWI trenches.  The field hospitals of the time were no better, as neither
were the ambulances.  They were perfect incubators and diseminators of
virus (modern hospitals are not much better) which, again, reinforced the
trench selection for virulence:  deathly ill hosts were thrown together in
close quarters with unifecteds - no quaranteen procedures. 

Just because the flu virus may be infecting a human host rather than
mixing within avian or swine doesn't mean that there is no
evolution/mutation going on. Influenza, having an RNA genome, is already a
high-rate mutator.  The fact that its genome is segmented only increases
its mutability - making recombination highly likely.  Technically, you are
not infected with a single, homogenous strain of influenza.  You are
infected with a swarm or quasispecies of virus.  Even if the infection is
initiated by a single virus, it will expand into a quasispecies with
multitudes of subtly and not so subtly differing variants (that's sort of
a redundant statement: "differing variants" :) ). 

Patrick





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