Concepedia

Publication | Closed Access

The Dynamics of Multiple Infection and the Evolution of Virulence

476

Citations

20

References

1995

Year

TLDR

Pathogen clones sharing a host create a conflict that favors higher virulence, and because virulence influences the force of infection, evolutionary dynamics must be coupled with population dynamics, yet existing models only consider first infections and are difficult to scale. The study examines host–pathogen interactions when hosts can be doubly infected. The model shows a feedback loop where frequent double infections drive higher virulence, but increased virulence lowers the force of infection, ultimately stabilizing virulence at a level determined by both within‑host competition and population‑level transmission.

Abstract

While for pathogen clones singly occupying a host it may pay to adopt a relatively avirulent host exploitation strategy, clones sharing a host have a conflict of interest that favors more virulent strategies. As the number of infections per host depends on the force of infection and the force of infection, in turn, depends on prevailing virulence, evolutionary analysis needs to be integrated with population dynamics. A full-fledged approach requires exceedingly large capacities for bookkeeping of the infection events and is therefore difficult to establish. In this article the host-pathogen interaction is studied for the simple case in which hosts may become at most doubly infected. It appears that evolution and population dynamics give rise to a feedback mechanism. When double infections are frequent, increased virulence is favored; but when pathogens become more virulent, the force of infection will decrease, favoring lower virulence again. Thus, evolutionarily stable strategy (ESS) virulence depends on the interaction within hosts as well as on the interaction at the population level. As current models of host-microparasite interactions take only first infections into account, they may be inappropriate for evolutionary analyses, which would require modeling of within-host competition between strains and thus of multiple infections.

References

YearCitations

Page 1