The dual role of autophagy during porcine reproductive and respiratory syndrome virus infection: A review

Autophagy is a highly conserved catabolic process that transports cellular components to lysosomes for degradation and reuse. It impacts various cellular functions, including innate and adaptive immunity. It can exhibit a dual role in viral infections, either promoting or inhibiting viral replication depending on the virus and the stage of the infection cycle. Porcine reproductive and respiratory syndrome virus (PRRSV) is a significant pathogen impacting the sustainable development of the global pork industry. Recent research has shown that PRRSV has evolved specific mechanisms to facilitate or impede autophagosome maturation, thereby evading innate and adaptive immune responses. These primary mechanisms involve viral proteins that target multiple regulators of autophagosome formation, including autophagy receptors, tethering proteins, autophagy-related (ATG) genes, as well as the functional proteins of autophagosomes and late endosomes/lysosomes. Additionally, these mechanisms are related to the post-translational modification of key components, viral antigens for presentation to T lymphocytes, interferon production, and the biogenesis and function of lysosomes. This review discusses the specific mechanisms by which PRRSV targets autophagy in host defence and virus survival, summarizes the role of viral proteins in subverting the autophagic process, and examines how the host utilizes the antiviral functions of autophagy to prevent PRRSV infection.