TLR7 is a key regulator of innate immunity against Japanese encephalitis virus infection

摘要: Toll-like receptor 7 (TLR7) known to recognize guanidine-rich ssRNA has been shown mount vital host defense mechanism against many viruses including flaviviruses. Signal transduction through TLR7 produce type-1 interferon and proinflammatory mediators, thereby initiating essential innate immune response in hosts. Systemic brain specific knock-down mice (TLR7(KD)) were generated using vivo-morpholinos. These then subcutaneously challenged with lethal dose of JEV (GP78 strain) subsequently analyzed for survival. Significant difference susceptibility between wild-type systemic TLR7(KD) was observed whereas, no infection seen brain-specific mice. decreases IFN-α antiviral proteins also both along increased viral loads their brain. Owing load, increases levels various cyto/chemokines, microglial activation infiltration peripheral cells observed. Immunocytochemistry RNA co-immunoprecipitation performed JEV-infected N2a or HT22 indicated endosomal localization confirmed interaction TLR7. Treatment imiquimod, a agonist, prior resulted Overall, our results suggest that the following promotes production generation state which might contribute protective effect infection.