Japanese encephalitis virus produces a CD4+ Th2 response and associated immunoprotection in an adoptive-transfer murine model

Japanese encephalitis virus produces a CD4+ Th2 response and associated immunoprotection in an adoptive-transfer murine model.

Japanese encephalitis is an acute infection of the central nervous system caused by Japanese encephalitis virus (JEV). The importance of an effective humoral response in preventing JEV infection has already been established, although the contribution of cellular immunity remains unclear. This study used an experimental murine model to understand the protective effects of cell-mediated immunity ...

Abrogated Inflammatory Response Promotes Neurogenesis in a Murine Model of Japanese Encephalitis

BACKGROUND Japanese encephalitis virus (JEV) induces neuroinflammation with typical features of viral encephalitis, including inflammatory cell infiltration, activation of microglia, and neuronal degeneration. The detrimental effects of inflammation on neurogenesis have been reported in various models of acute and chronic inflammation. We investigated whether JEV-induced inflammation has simila...

Japanese Encephalitis Virus: An Emerging Pathogen

Japanese Encephalitis Virus (JEV) is a flavivirus maintained in a zoonotic cycle which involves pigs, birds and Culex species of mosquitoes causing fatal encephalitis endemic most of Asia and as far as Australia from its putative origin in Indonesia and Malaysia. The principle vector is Culex mosquito, most important being Culex tritaenorhynchus, present in greatest density in rainy season (Jun...

Inflammation in Mice Is Mediated by CD4 An Adoptive Transfer Model of Allergic Lung

Antiviral and anti-inflammatory effects of rosmarinic acid in an experimental murine model of Japanese encephalitis.

Rosmarinic acid (RA) reduced the mortality of mice infected with Japanese encephalitis virus (JEV). Significant decreases in viral loads (P < 0.001) and proinflammatory cytokine levels (P < 0.001) were observed in JEV-infected animals treated with RA compared to levels in infected mice without treatment, at 8 to 9 days postinfection.