Abstract
Autophagy is an essential cellular process by which a cell degrades materials within its cytoplasm. Intracellular pathogens like viruses must deal with autophagy, either positively or negatively, for their own survival and replication. For some viruses, autophagy can even play proviral roles, helping their replication or dissemination. For other viruses, including noroviruses, the exact role of autophagy is more complex. This short review seeks to summarize the known interactions between autophagy, autophagy proteins and norovirus, and to address remaining questions relevant to these interactions.
Highlights
Autophagy is an essential cellular process by which a cell degrades materials within its cytoplasm
The interaction between autophagy and murine norovirus (MNV) is of particular interest, as it reveals a previously unexplored function of autophagy proteins in the control of intracellular pathogens in general, as well as functions that are not related to their capacity to facilitate degradative autophagy [4]
As neither microautophagy, which involves direct uptake of bulk cargo by lysosomes [10], nor chaperone-mediated autophagy (CMA), which degrades a small subset of proteins via recognition of a specific protein tag [11], have been implicated in host-pathogen defense against noroviruses, macroautophagy will primarily be discussed here
Summary
Autophagy is an essential cellular process by which a cell degrades materials within its cytoplasm. Characterization of interactions between RNA viruses and these proteins have demonstrated both proviral and antiviral roles for autophagy [9]. Poliovirus infection of human cells induces formation of double-membraned vesicles (DMVs), upon which viral replication takes place and which resemble autophagosomes.
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