Autophagy exerts an important effect on preserving homeostasis of cellular metabolism through degrading superfluous intracellular components. In addition, it serves as the defense mechanism for eliminating invading pathogens, such as viruses, by the host. The onset of a viral infection triggers autophagy, thereby initiating the innate immunity via the pattern recognition receptor pathways. As a result, interferons and other proinflammatory factors are produced. Furthermore, autophagy specifically targets immune components linked to viral particles for degradation. Through presenting virus-derived antigens to T lymphocytes, this process supports adaptive immunity. Nonetheless, certain viruses evolve mechanisms for inhibiting autophagy, enabling evasion of degradation and immune detection, since autophagy is frequently related to inflammatory diseases, including infections, autoimmune disorders, cancer, metabolic syndromes, neurodegenerative conditions, and cardiovascular and liver diseases. This review aims to summarize the current knowledge regarding the key molecules and specific molecular mechanisms that underlie the pattern recognition receptor signaling where autophagy is implicated during viral infections.
Xie et al. (Tue,) studied this question.
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