An adequate theory of the evolution of virulence must take into account the rate of establishment, in a given host, of new infections; the extent to which these competing pathogens differ in virulence; the rate of origin of new strains by mutation within a host; and the extent to which these new strains differ in virulence. From such considera- tions it should be possible to infer the expected levels of virulence for a given pathogen, assuming that conditions stay the same, which they never really do. The most important changes would be those that alter the means by which a pathogen reaches new hosts. If dispersal depends not only on a host’s survival but also on its mobility, any damage to the host is especially harmful to the pathogen. If you are so sick from a cold that you stay home in bed, you are unlikely to come into contact with many people that your virus might infect. If you feel well enough to be up and about, you may be able to disperse it far and wide. It is very much in a cold virus’s interest to avoid making you
favored by natural selection within a host. It exploits its host to maximize the current rate of dispersal of new individuals to new hosts. It may kill the
host quickly, but while the host lives it does better than any competing pathogen.