Just another comment on purpose

Olav Hungnes olavhung at idgonline.no
Tue Sep 17 10:09:50 EST 1996


iayork at panix.com (Ian A. York) wrote:
>Not so.  First, as far as many non-fatal viruses are concerned, a host is
>a one-shot case anyway (i.e. after a host is infected, it becomes immune,
>and the virus's progeny have no practical chance of re-infecting it; that
>individual host is out of the pool of susceptible individuals).  Since
>that host is of no more use to the virus, it cares not whether she lives
>or dies - it can't even detect the difference between a dead host and an
>immmune host.  (Sorry for the anthropomorphizing.  You know what I
>mean.)
Also, a virus being non-fatal is not necessarily a viral virtue,
rather a feature of the host's immune system.

>If the host dies, it leaves no more progeny; this might present a virus
>with a problem in the long run, but that's not necessarily the case.
>Hosts die anyway; individuals produce a more-than-replacement number of
>progeny.  The key is that the virus maintains a roughly steady level
>within the population over time.  A population can replace the ravages of
>a 100%-fatal virus.
Would you say that a finely balanced population (low early- and
mid-life mortality, roughly equal birth and death rate) is at at
particularly high risk of being decimated by aggressive pathogens?
Modern humans spring to mind, they are also very slow reproducers,
compared to viruses..

>One strategy for the virus is to allow the host to survive longer, and
>that may let it encounter more potential new hosts.  But there are many
>other also potentially successful strategies: it could survive longer
>outside the host, it could become more infectious (enhance the chance of
>infecting those new hosts it does encounter), it could cause the host to
>run around more to enhance the chance of meeting new hosts, and so on.

This is very well, what I have a problem understanding is how a virus
lineage can adapt to, or even maintain, a less aggressive (wrt. host
survival time or rate) strategy, at least if a reduced rate of virus
replication is the way to go.

Unless we have a cloning situation, i.e., all virus progeny within the
host is produced from one (slow-replication mutant) infectious unit,
then a slower-replicating genotype will lose out to its more
aggressive cousins infecting the same individual and have a lower
probability of transfer to new hosts, even if this genotype has a
better long-term strategy. The problem may share some characteristics
with how altruism can arise by natural selection. The road may
actually be easier for multi-cell organisms who usually multiply via
cloning events, i.e., haploid gamete stages. Our scenario will often
be more like cancer, where a majority of cells with a "good strategy"
of controlled growth can be overthrown by a single cell lineage that
has escaped such control.

Or would you say that transfer of virus between hosts often
functionally is a single-infectious-unit affair?

Another obstacle against achieving a
long-period-of-productive-infection strategy is of course the need to
evade immune responses.

>Rabies is close to, if not at, 100% fatal.  It's a highly successful
>virus, and its strategy hasn't changed over the centuries.  Rabid animals
>run around a lot, increasing their chances of meeting new hosts; they
>tend to be exciteable and snap at things, enhancing the infection of the
>virus in the salivary glands; and so on.
>
I seem to remember having read about a fungus that infects ants, and
then causes them to climb to the top of trees. There the ant is killed
by the replicating fungus, which then is able to get its airborne
spores spread more widely than if it just killed the ant lower down.
Is it conceivable that the alteration of ant behaviour is caused by
one mold-encoded substance? Other behaviour tricks used by
microorganisms to enhance spread are irritation of the mucosa to
induce coughing, sneezing, and induction of diarrhea.

Could one conceive an STD scenario with a virus/bacterium producing a
factor that stimulates mating behaviour? This could even result in
synergy.. Perhaps a virus could be the source of the ultimate
aphrodisiac?  :-)

Olav (forgive the smiley Ian, this is not a.f.u.) Hungnes

--
__________________________________________________________________________
Olav Hungnes                                   olavhung at idgonline.no
Natl.Inst.of Public Health, Dept.of Virology   ohungnes at embnet.uio.no
P.O.Box 4404 Torshov,                          phone: (+47)22 04 25 20
N-0403 OSLO, NORWAY                            FAX:   (+47)22 04 24 47





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