Research ArticleANTIVIRAL IMMUNITY

The host microRNA miR-301a blocks the IRF1-mediated neuronal innate immune response to Japanese encephalitis virus infection

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Sci. Signal.  14 Feb 2017:
Vol. 10, Issue 466, pp. eaaf5185
DOI: 10.1126/scisignal.aaf5185

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Fighting flavivirus infection

Japanese encephalitis virus (JEV), which is related to the Zika, West Nile, and dengue viruses, targets the central nervous system, causing viral encephalitis. Because of the high mortality rate in JEV-infected individuals and the neurological damage that afflicts survivors, effective antiviral therapies are urgently needed. Hazra et al. found that JEV infection of mouse and human neuronal cells increased the abundance of the microRNA miR-301a, which inhibited the cells from producing type I interferons (IFNs), cytokines that are critical to the antiviral immune response. One of the targets of miR-301a is the transcription factor IRF1, which is required for the expression of genes encoding type I IFNs. Treating JEV-infected mice with an inhibitor of miR-301a restored IRF1 abundance and function and led to increased type I IFN production, decreased viral replication, and increased survival. Together, these data suggest that targeting miR-301a may be an effective therapy against JEV infection.