Abstract

Virus-infected cells trigger a robust innate immune response and facilitate virus replication. Here, we review the role of autophagy in virus infection, focusing on both pro-viral and anti-viral host responses using a select group of viruses. Autophagy is a cellular degradation pathway operated at the basal level to maintain homeostasis and is induced by external stimuli for specific functions. The degradative function of autophagy is considered a cellular anti-viral immune response. However, autophagy is a double-edged sword in viral infection; viruses often benefit from it, and the infected cells can also use it to inhibit viral replication. In addition to viral regulation, autophagy pathway proteins also function in autophagy-independent manners to regulate immune responses. Since viruses have co-evolved with hosts, they have developed ways to evade the anti-viral autophagic responses of the cells. Some of these mechanisms are also covered in our review. Lastly, we conclude with the thought that autophagy can be targeted for therapeutic interventions against viral diseases.

Highlights

  • Academic Editor: Toshihiko TorigoeVirus infection triggers a robust cellular immune response via activating the pattern recognition receptors [1,2,3]

  • How autophagy regulates the cellular responses to virus infection is under-studied

  • Since many autophagy-related proteins have roles in regulating ubiquitination, it would be interesting to assess them in autophagy-independent cellular functions

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Summary

Introduction

Virus infection triggers a robust cellular immune response via activating the pattern recognition receptors [1,2,3]. In addition to triggering the anti-viral signaling pathways, the virus-infected cells can induce autophagy in the infected cells [6,7]. Basal level autophagy is required for maintaining cellular homeostasis, and autophagy is often induced in various disease conditions and infections [9]. The catabolic property of autophagy is primarily utilized as a cellular immune response to inhibit viral replication by degrading viral proteins. It is evident that viruses that do not rely on the machinery of autophagy for replication can still benefit from the components of the pathway. Autophagy pathway components can participate in autophagy-independent cellular functions.

Cellular Autophagy Pathway
Reticulophagy
Microautophagy
Lipophagy
Autophagy as an Anti-Viral Immune Response
Autophagy and the Interferon System
Autophagy
Viral Antagonism to Autophagy
Therapeutic Application of Autophagy in Virus Infection
Conclusions and Future Directions
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