Arboviruses cause encephalitis by infecting neurons of the host. Virus infection per se may cause death or dysfunction of neurons. The severity of the virus effect is dependent on the virulence of the virus and the maturity of the infected neuron. Neurons do not directly interact with T cells since they do not express MHC class I or class II antigens in vivo. Other cells such as microglia and perivascular macrophages probably present viral antigen to activated T cells coming to the brain from lymphoid organs. Infection elicits a local immune response that is characterized by mononuclear cell infiltration and local production of cytokines and antiviral antibody. The cytokines are primarily characteristic of type 2 T cells providing B cell help and macrophage deactivation. Control of virus replication is effected by antibody which does not eliminate infected cells. Therefore, viral RNA persists in the CNS, requiring continuous intraparenchymal production of antiviral antibody.
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