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In a recent paper in Science, April 14, 2000 issue: "Infectious History", I have begun to
explore the implications of the gross asymmetry in evolutionary pace of humans (and other
multicellulars) in contrast to microbes (here stipulated to include viruses.) If we judge the
intensity of natural selection by the fluctuation in population sizes per unit time, we already
see disparities of 8 or 10 powers of 10, even taking account of the greater gene complexity of
the macrobes. Nor are microbes bounded by speciation barriers to nearly the same degree, as
we see from the promiscuous exchange of plasmids. Obviously, macrobes would not have
survived if that evolutionary drive were directed to optimizing virulence and lethality of the
pathogen -- but the microbe could not then have survived either if it depended on that habitat.

However, most research in infectious disease has been focussed on mechanisms of virulence,
and host adaptations (mainly the immune system, invented 300 million years ago) for
countering that. Very little attention has been given to the parasites’ technology for
sustaining themselves as chronic inhabitants, as domesticators of their macrobial hosts --
which includes their shared interest in muting virulence. However, there are startling
examples, enough to substantiate the view that most encounters are driven by the parasites’
entelic goal of joint survival. In some cases, the immune system of the host is manipulated to
enhance resistance to superinfection by other invaders of the same or different species.
Macrobial evolution, perhaps excepting pandemic disease of unusual ferocity (malaria) is just
too slow to add more than a few nuances to the encounters. A year in microbial history
matches all of primate, perhaps mammalian evolution. It may broaden our horizons if we
think of the human as a superorganism, with an extended genome as comprising

a) karyome -- chromosome set
b) chondriome -- mitochondria
c) microbiome -- entourage of microbial flora that

we Carry in and on us, perhaps as endosymbionts, but also on
our skin, gut lumen, mucosal surfaces, and elsewhere.

Each of these components can have an important impact on the outcome of our encounters
with infection (and reinfection), as well as on nutrition and other phenotypes.