"Mike Williams" <nospam@[EMAIL PROTECTED]
> wrote in message
news:PhGIqpDmWSuHFw1e@[EMAIL PROTECTED]
> Wasn't it Carey Sublette who wrote:
>>
>>The difficulty is in large part due to disease virulence being an
>>extremely
>>specialized ecological niche.
>
> Diseases tend evolve away from high virulence because killing the host
> also means death for the disease organisms. Incapacitating the host
> reduces the number of contacts, thereby reducing the ability of the
> disease to propagate.
The term "virulence" refers to the ability to cause disease, and thus
contains the notions of contagiousness and the ability to cause disease
symptoms. A highly virulent disease does not necessarily kill its host
with
significant probability, in fact most don't. Influenza epidemics kill
people, a lot in fact as humans count it, but far too few to have any
relevance for disease transmission. Even host incapacitation is
questionable
as being effective in reducing transmission since infectious phases often
preceed severe disease symptoms, and in high population density
environments
(cities - where nearly half the world lives) reduced mobility may have
little relevance to maintaining the transmission chain.
> High virulence tends to occur in situations where the disease organism
has
> evolved in a different host population. That could be a different
species
> or an isolated population of the same species. The original host
> population gradually evolves resistance to the disease, and the disease
> evolves to increase the strength of its attack on the host. High
virulence
> occurs when the disease jumps to a different population which has not
> evolved such resistance.
That's a pattern that occurs, yes, but the notion is commonly over
generalized.
HIV crossed over from a natural non-numan reservoir, true, but is
contagiousness and lethality appears to have *increased* as it adapted to
its human host. This is possible due to the very long latency for full
AIDS,
but it illustrates that what is involved is the complex balance between
rate
of disease development, speed of transmission, and role of disease
symptoms
(if any) in the actual transmission process, i.e. the disease ecology.
In some diseases the symptoms of the disease have a direct role in
transmission - i.e. the pustules in smallpox, the cough in diptheria and
other respiratory diseases. In these cases there may be no long-term
tendency to become milder since this would interfere with disease
transmission.
There are also microbes that have been around humans a long, long time and
are even common infections in some cases, but only rarely turn into severe
diseases. For example culturing Neisseria meningitidis from symptom-free
humans is fairly common. This bacteria only infects humans; there is no
animal reservoir, yet occasionally it turns into a killer epidemic.
The processes are complex, and so is the balances between them. In any
case
my point is well established - the fallacy of assuming that if microbe X
"causes disease" then if one obtains microbe X one can use it to cause
disease. With most microbes, very rarely will microbe X actually be an
effective disease causing strain.
Biowarfare programs, BTW, liked to obtain their specimens from people who
were really sick - thus proving the organisms pathogenicity. Maintaining
that trait in lab culture is still a problem.
Finally, many diseases of interest to biowarfare programs aren't even
transmissible between people. This is actually a favorable trait for most
weapons uses since the idea is infect a target population through weapon
dispersal, not have it turn into an uncontrolled epidemic. Examples are
vector borne-diseases (yellow fever, dengue, rocky mountain spotted
fever),
ones picked up from the enviroment (San Joaquin Valley Fever), or ones
normally only transmitted from infected animals (glanders).
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