LAUSR

Autophagy, a conserved lysosomal degradation pathway, can degrade intracellular waste, such as damaged organelles or misfolded proteins, to meet the metabolic needs of cells and maintain the homeostasis of the intracellular environment (1). In addition, autophagy also plays an essential role in immunity. First, autophagy can be induced by invading virus and provides a way for the host to limit or eliminate the intracellular virus; second, autophagy can also control inflammation by regulating interactions with natural immune signaling pathways, removing endogenous inflammasome agonists, and influencing the secretion of immune mediators; third, autophagy involves in antigen presentation and T polarization (2, 3). The virus typically enters host cells via endocytosis and thus remains enclosed in the endosomes during the early stages of infection, making it difficult to identify by the host cellular autophagy. There is unknown how the virus can be specifically identified as selective autophagy cargo so as to be eliminated by host cellular autophagy and how does virus-induced autophagy occur in mammalian cells. Recently, Dong et al. found that the endosomal protein sorting nexin 5 (SNX5) is critically required for virus-induced, but not for other factor induced autophagy (4).