Conserved amino acids 193-324 of non-structural protein 3 are a dominant source of peptide determinants for CD4+ and CD8+ T cells in a healthy Japanese encephalitis virus-endemic cohort.

Our earlier identification of the non-structural protein 3 (NS3) of Japanese encephalitis virus (JEV) as a dominant CD4+ as well as CD8+ T cell-eliciting antigen in a healthy JEV-endemic cohort with a wide HLA distribution implied the presence of several epitopes dispersed over the length of the protein. Use of various truncated versions of NS3 in lymphocyte stimulation and interferon (IFN)-gamma secretion assays revealed that amino acids (aa) 193-324 of NS3 were comparable with, if not superior to, the full-length protein in evoking Th1 responses. The potential of this 14.

Impaired T helper 1 function of nonstructural protein 3-specific T cells in Japanese patients with encephalitis with neurological sequelae.

Japanese encephalitis virus (JEV) is the principal cause of viral encephalitis. The predominance of children among patients with encephalitis in areas where JEV is endemic that do not have immunization programs suggests that acquired immunity is critical in protecting adults against symptomatic JEV encephalitis. We characterized and compared the T cell response to nonstructural (NS) protein 3 between healthy individuals naturally exposed to JEV and patients in the convalescent phase of JEV encephalitis.

Cell-mediated immune responses in healthy children with a history of subclinical infection with Japanese encephalitis virus: analysis of CD4+ and CD8+ T cell target specificities by intracellular delivery of viral proteins using the human immunodeficiency virus Tat protein transduction domain.

Japanese encephalitis virus (JEV), a single-stranded positive-sense RNA virus of the family Flaviviridae, is the major cause of paediatric encephalitis in Asia. The high incidence of subclinical infections in Japanese encephalitis-endemic areas and subsequent evasion of encephalitis points to the development of immune responses against JEV. Humoral responses play a central role in protection against JEV; however, cell-mediated immune responses contributing to this end are not fully understood.