Lytic Cycle of Toxoplasma gondii: 15 Years Later

Abstract

Toxoplasmosis is the clinical and pathological consequence of acute infection with the obligate intracellular apicomplexan parasite Toxoplasma gondii. Symptoms result from tissue destruction that accompanies lytic parasite growth. This review updates current understanding of the host cell invasion, parasite replication and eventual egress that comprise the lytic cycle, as well as the ways T. gondii manipulates host cells to assure survival. Since the publication of a previous iteration of this review 15 years ago, important advances have been made in our molecular understanding of parasite growth and mechanisms of host cell egress, and knowledge of the parasite’s manipulation of the host has rapidly progressed. Here we cover molecular advances and current conceptual frameworks that include each of these topics, with an eye to what might be known 15 years from now.

Calcium signaling and the lytic cycle of the Apicomplexan parasite Toxoplasma gondii

“…Some of the most devastating effects of toxoplasmosis are the result of the parasite lytic cycle (Fig. 1), which starts when the tachyzoite attaches and invades a host cells, replicates inside a parasitophorous vacuole and egresses to find another host cell to invade and re-start the cycle [9, 10]. …”

“…Inhibition (using pharmacological agents) or disruption (using knockouts or conditional depletion of core components) of the glideosome has been known to adversely affect the lytic cycle events of egress, extracellular motility, and invasion thus highlighting its significance across the lytic cycle [10, 125]. Egress results from the initiation of the glideosome and parasites will continue to be actively motile until invasion of new host cells suggesting that extracellular motility serves as the bridge connecting egress and invasion [10]. As an intracellular parasite, T. gondii must replicate inside host cells; and as such, glideosome activation must be tightly regulated across time and space [91].…”

Protozoan Parasites and Type I IFNs

“…After ingestion of T. gondii oocysts by an intermediate host, the parasite transforms into tachyzoites that rapidly undergo multiplication within the parasitophorous vacuole inside various cell types. If the infection is controlled, parasites are retained in tissue cysts; if not, they can cause a systemic lethal disease (54, 55). …”

Toxoplasma gondii Tissue Cyst: Cyst Wall Incorporation Activity and Matrix Cytoskeleton Proteins Paving the Way to Nutrient Acquisition

“…Actin is a highly conserved microfilament protein that plays an important role for gliding motility and in T. gondii tachyzoites host cell invasion [39]. By indirect immunofluorescence, actin has been reported to be primarily concentrated in the anterior third of the tachyzoite and in a diffuse staining pattern throughout the cytoplasm [40,41], our immunofluorescence for Toxoplasma gondii Tissue Cyst: Cyst Wall Incorporation Activity and Matrix Cytoskeleton... http://dx.doi.org/10.5772/intechopen.68202 actin in the bradyzoite stage revealing the same staining pattern.…”