Abstract
Viruses have played an important role in human evolution and have evolved diverse strategies to co-exist with their hosts. As obligate intracellular pathogens, viruses exploit and manipulate different host cell processes, including cellular trafficking, metabolism and immunity-related functions, for their own survival. In this article, we review evidence for how autophagy, a highly conserved cellular degradative pathway, serves either as an antiviral defense mechanism or, alternatively, as a pro-viral process during virus infection. Furthermore, we highlight recent reports concerning the role of selective autophagy in virus infection and how viruses manipulate autophagy to evade lysosomal capture and degradation.
Highlights
To co-exist with their hosts viruses have evolved diverse mechanisms to exploit cellular processes and to evade from host defenses
In contrast to proteasomal degradation that targets ubiquitinated proteins, autophagy is mediated by the lysosome, which serves as an end point degradative organelle
ULK1 and ULK2 complexes that are crucial for induction of autophagy, PI3Kinase-Beclin1 complexes, are required for autophagosome formation, the delivery of membranes to the forming autophagosome is mediated by mammalian Atg9 and two conjugation systems: LC3-II and Atg12±Atg5±Atg16L complex, which are required during elongation and expansion of the phagophore
Summary
To co-exist with their hosts viruses have evolved diverse mechanisms to exploit cellular processes and to evade from host defenses. Autophagy is a catabolic process that maintains cellular homeostasis by degradative removal of damaged or excess cellular organelles and protein aggregates from the cytoplasm, thereby enabling cell survival Both cell culture and in vivo studies revealed the fundamental roles of autophagy in numerous diseases, including cancer or neurodegeneration, in aging, and in innate and adaptive immunity to pathogen infection. In contrast to CMA, macroautophagy (called autophagy ) involves sequestration of intact organelles (e.g., mitochondria) and portions of the cytosol via a membrane referred to as the phagophore or isolation membrane [3,4] This phagophore expands to form double-membrane vesicles, termed autophagosomes [3,4]. ULK1 and ULK2 complexes that are crucial for induction of autophagy, PI3Kinase-Beclin complexes, are required for autophagosome formation, the delivery of membranes to the forming autophagosome is mediated by mammalian Atg (mAtg9) and two conjugation systems: LC3-II and Atg12±Atg5±Atg16L complex, which are required during elongation and expansion of the phagophore
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