ArticleJournal of virology2011
Pivotal role of antibody and subsidiary contribution of CD8+ T cells to recovery from infection in a murine model of Japanese encephalitis.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 81 citations in OpenAlex.
- Human T cell responses to Japanese encephalitis virus in health and disease.The Journal of experimental medicine · 2016Trial
- Article
- Recombinant Japanese Encephalitis Virus Envelope Antigen Presented on CoPoP Liposomes Elicits Cellular Immunity and Protects Mice From Lethal Challenge.Immune network · 2026Article
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- mRNA Vaccine Against Japanese Encephalitis Virus Genotype IV Protects Against Lethal Infection.Viruses · 2026Article
- Balancing functions of regulatory T cells in mosquito-borne viral infections.Emerging microbes & infections · 2024Review
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- Epitope(s) involving amino acids of the fusion loop of Japanese encephalitis virus envelope protein is(are) important to elicit protective immunity.Journal of virology · 2024Article
- Myeloid-Derived Suppressor Cells Induce Exhaustion-Like CD8International journal of biological sciences · 2024Article
- Novel approaches for the rapid development of rationally designed arbovirus vaccines.One health (Amsterdam, Netherlands) · 2023Article
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Rational Development of Live-Attenuated Zika Virus Vaccines.Pathogens (Basel, Switzerland) · 2023Review
- Review
- Comparison of Wild Type DNA Sequence of Spike Protein from SARS-CoV-2 with Optimized Sequence on The Induction of Protective Responses Against SARS-Cov-2 Challenge in Mouse Model.Human vaccines & immunotherapeutics · 2022Article
- Identification of a promiscuous conserved CTL epitope within the SARS-CoV-2 spike protein.Emerging microbes & infections · 2022Article
- Review
- The Comparison of Inflammatory Cytokines (IL-6 and IL-18) and Immune Cells in Japanese Encephalitis Patients With Different Progression.Frontiers in cellular and infection microbiology · 2022Article
- The difference in CD4Frontiers in immunology · 2022Article
- Pre-treatment with Scopolamine Naturally Suppresses Japanese Encephalitis Viral Load in Embryonated Chick Through Regulation of Multiple Signaling Pathways.Applied biochemistry and biotechnology · 2021Article
- A genetically stable Zika virus vaccine candidate protects mice against virus infection and vertical transmission.NPJ vaccines · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The immunological correlates for recovery from primary Japanese encephalitis virus (JEV) infection in humans and experimental animals remain poorly defined. To investigate the relative importance of the adaptive immune responses, we have established a mouse model for Japanese encephalitis in which a low-dose virus inoculum was administered into the footpads of adult C57BL/6 mice. In this model, ~60% of the mice developed a fatal encephalitis and a virus burden in the central nervous system (CNS). Using mice lacking B cells (μMT(-/-) mice) and immune B cell transfer to wild-type mice, we show a critically important role for humoral immunity in preventing virus spread to the CNS. T cell help played an essential part in the maintenance of an effective antibody response necessary to combat the infection, since mice lacking major histocompatibility complex class II showed truncated IgM and blunted IgG responses and uniformly high lethality. JEV infection resulted in extensive CD8(+) T cell activation, judged by upregulation of surface markers CD69 and CD25 and cytokine production after stimulation with a JEV NS4B protein-derived H-2D(b)-binding peptide and trafficking of virus-immune CD8(+) T cells into the CNS. However, no significant effect of CD8(+) T cells on the survival phenotype was found, which was corroborated in knockout mice lacking key effector molecules (Fas receptor, perforin, or granzymes) of cytolytic pathways triggered by T lymphocytes. Accordingly, CD8(+) T cells are mostly dispensable for recovery from infection with JEV. This finding highlights the conflicting role that CD8(+) T cells play in the pathogenesis of JEV and closely related encephalitic flaviviruses such as West Nile virus.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.