Toxoplasma

Abstract

Toxoplasma gondii is the most widespread intracellular parasite of warm-blooded vertebrates including humans. Infections are mostly asymptomatic or benign in immunocompetent hosts but can be life threatening in immunocompromised individuals and in fetuses after vertical transmission. T. gondii has become a model organism for intracellular parasitism as well as for other Apicomplexa. Genome and transcriptome data for different T. gondii strains are publically available, and powerful forward and reverse genetic tools have been developed. Here we summarize molecular and cellular features of T. gondii that are critical for the biology of the parasite and its interaction with the host. This includes characteristics of the three parasite genomes and how gene expression may be controlled. Examples for T. gondii-specific metabolic features including metabolic pathways of the apicoplast are highlighted. Being an intracellular parasite, the mechanism of host cell invasion is also of major interest. It involves adhesins of the SAG-related sequence protein family, sequential secretion of a large number of proteins from three characteristic secretory organelles (i.e., micronemes, rhoptries, and dense granules), and a unique form of motility accomplished by the “glideosome” multi-protein complex. Polymorphic excretory-secretory proteins from the rhoptries and the dense granules injected into the host cell also extensively modify host responses and determine parasite virulence. Finally, conversion from the proliferative tachyzoite to the dormant bradyzoite stage is critical for the establishment of a chronic infection and allows host (and parasite) survival and transmission to new hosts.