The apicomplexan parasite
Toxoplasma gondii
is unusual in being able to infect almost any cell from almost any
warm-blooded animal it encounters. This extraordinary host-range contrasts with its far more particular cousins
such as the various species of the malaria parasite
Plasmodium where each species of parasite has a single genus
or even species of host that it can infect. Genetic and genomic studies have revealed a key role for a number of gene
families in how Toxoplasma invades a host cell, modulates gene expression of that cell and successfully evades the
resulting immune response. In this review, I will explore the hypothesis that a combination of sexual recombination
and expansion of host range may be the major driving forces in the evolution of some of these gene families and the
specific genes they encompass. These ideas stem from results and thoughts published by several labs in the last few
years but especially recent papers on the role of different forms of rhoptry proteins in the relative virulence of F1
Toxoplasma progeny in a particular host species (mice).