It is well known that JEV infection causes microglial activation. Activated microglia releases an array of chemical mediators that are detrimental for the neurons in brain [24] . Since there was reduction in the production of infective viral particles following 39 and 59 MO treatments, we studied the effect on microglial pathophysiology in mouse brain. Our results show that there was significantly reduced number of activated microglia in the brain sections of both 39 and 59 MO-treated animals as compared to only JEV-infected or JEV-infected and SC-MO treated animals. Since there were little or no activation of microglia, proinflammatory cytokine levels in the brain were found to be significantly downregulated. Histochemical staining also revealed that neuronal population and morphology remained largely unaffected in 39 and 59 MO-treated animals' brains as compared to only JEV-infected or JEV-infected and SC-MO treated animals.