Insights into the immunopathogenesis during Japanese encephalitis virus infection

The magnitude of Japanese encephalitis occurrence is escalating from last few years. Despite the availability of vaccine, new cases are arising; therefore it is important to look for better prevention strategies to control JEV. In order to achieve, one has to explore the various ways of immune evasion strategies employed by JEV. Persistence of JEV in the infected target cells by accumulation of autophagosome is the novel mechanism to escape host immune anti-viral response. JEV nterferes with the IFN signaling pathway by inhibiting nuclear translocation of STAT2 which is mediated by NS5 protein. JEV infection results in the up-regulation of MHC-I on the surface of infected target cells. On the other hand it also activates the cellular autophagy to diminish the innate immune response to promote the cell survival. JEV infects the central nervous system via trans-migrating neutrophils, which can breach the blood brain barrier. Detection of viral RNA via RIG-I has suggested the activation of NF-κB pathway in the infected neurons. As a result of the activation, elevated level of pro-inflammatory cytokines and chemokines contributes to the inflammation of the brain. The primary focus of this review is to discuss the immunopathogenesis during JEV infection including the future perspectives that might be crucial in understanding the involvement of various cytokines and chemokines in the development of neuroinflammation and encephalitis.