Japanese encephalitis virus activates autophagy as a viral immune evasion strategy.

Rui Jin, Wandi Zhu, Shengbo Cao, Rui Chen, Hui Jin, Yang Liu, Shaobo Wang, Wei Wang, Gengfu Xiao

PloS one 2013

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In addition to manipulating cellular homeostasis and survivability, autophagy also plays a crucial role in numerous viral infections. In this study, we discover that Japanese encephalitis virus (JEV) infection results in the accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II) protein and GFP-LC3 puncta in vitro and an increase in autophagosomes/autolysosomes in vivo. The fusion between autophagosomes and lysosomes is essential for virus replication. Knockdown of autophagy-related genes reduced JEV replication in vitro, as indicated by viral RNA and protein levels. We also note that JEV infection in autophagy-impaired cells displayed active caspases cleavage and cell death. Moreover, we find that JEV induces higher type I interferon (IFN) activation in cells deficient in autophagy-related genes as the cells exhibited increased phosphorylation and dimerization of interferon regulatory factor 3 (IRF3) and mitochondrial antiviral signaling protein (MAVS) aggregation. Finally, we find that autophagy is indispensable for efficient JEV replication even in an IFN-defective background. Overall, our studies provide the first description of the mechanism of the autophagic innate immune signaling pathway during JEV infection.

Citation

Rui Jin, Wandi Zhu, Shengbo Cao, Rui Chen, Hui Jin, Yang Liu, Shaobo Wang, Wei Wang, Gengfu Xiao. Japanese encephalitis virus activates autophagy as a viral immune evasion strategy. PloS one. 2013;8(1):e52909