Generation of ROS with the generation of oxidative damage has been implicated in neurodegenerative diseases and in the degradation of nervous system functions and are also reported to increase following JEV infection [22] . Increase in ROS levels initiates various responses within the cell, including damage to proteins, DNA and lipid [36] . In this study, ROS levels were found to be many-fold increased in JEV-infected or JEV-infected and SC-MO treated animals that were then found to be counteracted by the treatment of 39 and 59 MO. The levels of stress related proteins such as SOD-1, HSP-70 and TRX where also found to be positively modulated following 39 and 59 MO treatment. NO is a known antagonist of JEV. It has been shown that NO inhibits JEV infection by preventing viral replication [37] . In our study NO levels were increased in the brain in response to JEV infection possibly due to the upregulation of inducible nitric oxide synthase (iNOS). Treatments with 39 and 59 MO caused a decrease of NO to basal levels as observed in Sham-treated animals.