To our knowledge, this study is the first report showing that EV71 infection activates learn more JNK1/2 and p38 MAPK pathways in iDCs and leads to increased viral yield and proinflammatory cytokine secretions. Moreover, inhibition of JNK1/2 and p38 MAPK pathways could effectively reduces viral replication and cytokine release, supporting the idea that the activation of these two pathways are important for EV71 infection. We speculate that JNK1/2 and p38 MAPK regulate viral replication by acting at certain specific steps of viral replication cycle, including attachment, entry, gene transcription, protein expressions, and
assembly, as well as viral pathogenesis. However, the underlying mechanisms need to be further studied in vitro or in vivo to highlight JNK1/2 or p38 MAPK as a potential broad antiviral molecular target for treatment of EV71 infection. Acknowledgments The authors would like to thank Guanghua Luo, Ming Li, Rong Wang and Haifeng Deng for their help in flow cytometry and statistical analysis. This research project was supported by the National Natural Science LY2874455 cell line Foundation of
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