Abstract
Autophagy is a conservative lysosomal catabolic pathway commonly seen in eukaryotic cells. It breaks down proteins and organelles by forming a two-layer membrane structure of autophagosomes and circulating substances and maintaining homeostasis. Autophagy can play a dual role in viral infection and serve either as a pro-viral factor or an antiviral defense element dependent on the virus replication cycle. Recent studies have suggested the complicated and multidirectional role of autophagy in the process of virus infection. On the one hand, autophagy can orchestrate immunity to curtail infection. On the other hand, some viruses have evolved strategies to evade autophagy degradation, facilitating their replication. In this review, we summarize recent progress of the interaction between autophagy and viral infection. Furthermore, we highlight the link between autophagy and SARS-CoV-2, which is expected to guide the development of effective antiviral treatments against infectious diseases.
Highlights
Autophagy is an evolutionary conserved lysosome-dependent cellular metabolic pathway in eukaryotic cells by degrading senescent organelles and long-lived proteins into small molecules such as peptides or amino acids through which the material recycling and intracellular homeostasis can be maintained (Chiang, Terlecky et al, 1989; Rubinsztein, Marino et al, 2011; Wei, Liu et al, 2018; Levine and Kroemer 2019)
It can present viral antigens processing to MHC molecules to activate adaptive immunity in organisms. It can transport the virus in the cytoplasm to the lysosome by heterologous phagocytosis, which plays a role in resisting virus infection
Viruses can promote their infection by inhibiting autophagy, interacting with autophagy proteins, and even using autophagy as a replication site
Summary
Autophagy is an evolutionary conserved lysosome-dependent cellular metabolic pathway in eukaryotic cells by degrading senescent organelles and long-lived proteins into small molecules such as peptides or amino acids through which the material recycling and intracellular homeostasis can be maintained (Chiang, Terlecky et al, 1989; Rubinsztein, Marino et al, 2011; Wei, Liu et al, 2018; Levine and Kroemer 2019).
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