Herpesviruses and autophagy: An intracellular conflict

Herpesviruses are a class of viruses capable of causing various diseases in humans and animals. These pathogens have the ability to remain latent within the host cell for extended periods, often remaining dormant until immune function is compromised. Extensive research indicates that autophagy, as a key intracellular defense mechanism, is closely associated with the herpesvirus life cycle. Following cellular invasion, herpesviruses evade immunity and sustain infection by modulating autophagy formation, blocking autophagy-lysosome fusion, or selectively degrading key immune molecules via autophagy. Concurrently, autophagy exerts antiviral effects under specific conditions by restricting viral replication through receptor-mediated degradation or non-canonical pathways. This review summarizes recent advances in herpesvirus-autophagy interactions, outlines the commonalities and unique features of viral autophagy regulation, and explores its impact on viral life cycles and host immune responses. The theoretical foundations for identifying novel antiviral targets and developing precision interventions for herpesvirus-related diseases are provided.