On 16 Mar 1995 bhjelle at unm.edu wrote:
>> For viruses, as opposed to certain parasites, there is quite
> a bit of support for the notion of adaptation toward low
> pathogenicity for the native host, while having significant
> pathogenicity for non-native hosts.ri.
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
field hospitals and ambulance service of the time also contributed greatly
to the ultimate development of a flu variant that killed 20 million people
within a single year. There was no pressure against a supervirulent form,
no disadvantage, so under these circumstances, those variants won out.
The same can go for a sexually transmitted disease. If partner exchange
rate is low, slow acting and relatively benign variant viruses are
selected for but increase partner exchange frequency and you automatically
select for more virulent forms. If exchange frequency is really high,
then high pathogenicity and rapid onset are favored until the frequency
drops, whether by choice or as a matter of course: the loss of healthy,
living partners to disease.
Change the selective pressures to those that allow rapid transmission
from host to host and, no matter how long a virus has been enjoying a
host's hospitality, the more virulent forms will begin to predominate.