Abstract
Recent years have witnessed a great gain in knowledge regarding parasite–host cell interactions during Plasmodium liver stage development. It is now an accepted fact that a large percentage of sporozoites invading hepatocytes fail to form infectious merozoites. There appears to be a delicate balance between parasite survival and elimination and we now start to understand why this is so. Plasmodium liver stage parasites replicate within the parasitophorous vacuole (PV), formed during invasion by invagination of the host cell plasma membrane. The main interface between the parasite and hepatocyte is the parasitophorous vacuole membrane (PVM) that surrounds the PV. Recently, it was shown that autophagy marker proteins decorate the PVM of Plasmodium liver stage parasites and eliminate a proportion of them by an autophagy-like mechanism. Successfully developing Plasmodium berghei parasites are initially also labeled but in the course of development, they are able to control this host defense mechanism by shedding PVM material into the tubovesicular network (TVN), an extension of the PVM that releases vesicles into the host cell cytoplasm. Better understanding of the molecular events at the PVM/TVN during parasite elimination could be the basis of new antimalarial measures.
Highlights
Host immune responses put a strong evolutionary pressure on pathogens including viruses, bacteria and parasites
While canonical autophagy serves as an important nutrient source during Plasmodium liver stage development, mechanisms related to either selective autophagy or LC3-associated phagocytosis (LAP) represent an intracellular immune response, which we summarize under the term Plasmodium-associated autophagy-related (PAAR) response (Fig. 1)
IFN-γ -mediated LAP response depends on Beclin 1, a member of the PI3KC3 core complex, and the ubiquitin-like conjugation system to promote LC3-PE incorporation and recruitment of acid vesicles to the parasitophorous vacuole membrane (PVM)
Summary
Host immune responses put a strong evolutionary pressure on pathogens including viruses, bacteria and parasites. Plasmodium liver stage parasites replicate within the parasitophorous vacuole (PV), formed during invasion by invagination of the host cell plasma membrane. It was shown that autophagy marker proteins decorate the PVM of Plasmodium liver stage parasites and eliminate a proportion of them by an autophagy-like mechanism.
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