Viruses are a type of pathogen that is entirely dependent on the host for life and multiplication. As a result, to live, the virus evolved an immunological escape strategy from the complement system by releasing a large number of inhibitory proteins/cytokines. However, because it is a multicomponent system, the complement system can be an adversary in conditions of Flavivirus infection, including JE. During JEV infection, the host cell recruits a humoral immune system, which is an important factor in the process of human infection defense. Upon infection by the virus, host humoral responses commence the process by identifying the virus and recruiting Th cells which react to viral antigens. Cell-mediated immunity is critical in the clearance or elimination of JEV-infected cells. IFN-γ and IL-2, which are secreted by T-helper (Th) or T-cytotoxic (TC) cells, are the primary cytokines in this mechanism. IL-2 aids in the transformation of naive T cells into virus-specific cytotoxic T lymphocytes (CTLs), which then kill virus-infected cells. Subsequently, CTLs transfer viral antigens or proteins to B cells with the assistance of macrophages. Th cells that have been triggered produce cytokines such as IFN-γ, IL-2, IL-6, and TNF-α, which disrupt the cellular activities of JEV and thereby protect the host from the virus. These effector chemicals are generated by Th1, CD4+, and CD8+ Tc cells, in order to induce cell-mediated immune responses. Among these cytokines, both IFN-γ and TNF-α may aid in peripheral viral clearance but not in CNS virus clearance.