A latent ability to persist: differentiation in Toxoplasma gondii

Abstract

A critical factor in the transmission and pathogenesis of Toxoplasma gondii is the ability to convert from an acute disease-causing, proliferative stage (tachyzoite), to a chronic, dormant stage (bradyzoite). The conversion of the tachyzoite-containing parasitophorous vacuole membrane into the less permeable bradyzoite cyst wall allows the parasite to persist for years within the host to maximize transmissibility to both primary (felids) and secondary (virtually all other warm-blooded vertebrates) hosts. This review presents our current understanding of the latent stage, including the factors that are important in bradyzoite induction and maintenance. Also discussed are the recent studies that have begun to unravel the mechanisms behind stage switching.

Keywords: Bradyzoite; Differentiation; Encystation; Epigenetics; Gene regulation; Immunity; Latency; Tachyzoite; Toxoplasma; Toxoplasmosis.

Fig. 1

5-day-old, in vitro bradyzoite cyst induced under alkaline conditions, stained with fluorophore-linked lectin from Dolichos biflorus (red), which binds to the polysaccharide-rich cyst wall. Blue: 4′,6-diamidino-2-phenylindole, DAPI (nucleus). Scale bar 10 µm. Labeled schematic depicts the stained tissue cyst in the infected host cell