How Toxoplasma and malaria parasites defy first, then exploit host autophagic and endocytic pathways for growth. (December 2017)

• Record Type: Journal Article
• Authors: Coppens, Isabelle
• Is Part Of: Current opinion in microbiology. Volume 40(2017)
• Page Start: 32
• Page End: 39
• Publication Date: 2017-12
• Subjects: Microbiology -- Periodicals; 579.05
• DOI: 10.1016/j.mib.2017.10.009
• Languages: English
• ISSNs: 1369-5274

Abstract

Highlights: A LC3-associated phagocytic-like pathway is activated by host cells to control Apicomplexa. LC3 is directly inserted into the PV membrane. LC3-positive PV membrane is stripped by IRG/GBP, or fuse with lysosomes for degradation. Toxoplasma can prevent LC3 deposition at the PV and Plasmodium remove LC3 from the PV. Surviving Apicomplexa derive benefit from the nonselective autophagy and heterophagy for replication. Abstract : Infections caused by the apicomplexan parasites Plasmodium and Toxoplasma are wide-spread, life-threatening and therapeutically challenging. These pathogens are obligate intracellular microorganisms that invade mammalian cells by forming a self-made niche, the parasitophorous vacuole that is impervious to host lysosomal fusion. Shortly after invasion, a noncanonical xenophagic pathway resembling LC3-associated phagocytosis is activated by the host cell to control infections. However, Plasmodium and Toxoplasma have elaborated strategies to avoid clearance by the sentinel activities of the host autophagic system. After this initial confrontation, replicating Plasmodium and Toxoplasma adeptly usurp, for their own benefit, host autophagic and endocytic structures by attracting these organelles to their vacuole, likely to access their nutrient-rich content. The pleomorphic function of the autophagy system, from microbial defense to nutrient supply, is reflected by its ambivalent role during the intracellular development of these apicomplexan parasites.