Résumé
For many host‐parasite interactions, virulence is necessarily affected by population densities, transmission biology of the parasite, and proliferation of the parasite at the expense of its host. Attempts to experimentally demonstrate genetic correlations involving virulence therefore need to employ protocols controlling for variation in the number of successful infections (i.e., the end‐point of transmissibility). If protocols are not controlled, then correlations may be spurious, as appears to be the case in recent experimental studies by Ebert (1994) and Ebert and Magnin (1997). There is a need to explore the modes of the evolution of each of the many sequential steps in nonsymbiotic and symbiotic phases of host‐parasite associations and the implication of such evolution for overall virulence. I argue that it is the interdependence of these sequential steps (and not overall virulence) that should be at the center of attempts to establish genetic correlations.