Activation of pNFkB regulates apoptotic genes, especially the TRAF1 and TRAF2, and thereby checks the activities of the caspases, which are central to most apoptotic processes. JEV is known to activate pNFkb via a PI3K-dependent pathway in the brain of infected animals, which is associated with apoptosis [38] . JEV infection has also been shown to activate stress kinases, which in turn results in activation of ERK1/2, and p38 MAPK pathway leading to apoptotic death of neurons [39] . In accordance with the established results, here also we found that there was similar activation pattern of these molecules in JEV-infected and JEVinfected and SC-MO treated animal brain samples. Treatment with the MOs resulted in abrogation of those changes that led to greater survivality of brain neurons as observed by histochemical staining. Activation of p38MAPK is also related to the transcriptional activation of proinflammatory genes in the brain [40] . Thus the decrease in phophoP38 MAPK levels correlates with the decreased levels of proinflammatory cytokine levels in obtained from the brain.