ArticlePloS one2011
Mice with different susceptibility to Japanese encephalitis virus infection show selective neutralizing antibody response and myeloid cell infectivity.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Spatial transcriptomics uncovers vasculature-centered cellular interactions driving Japanese encephalitis progression in a mouse model.Nature communications · 2026Article
- Inflammatory & Apoptotic Factor Fluctuations Associated with Japanese Encephalitis Virus Infection in Transgenic IFNAR1Current microbiology · 2024Article
- The Role of Chitinase 3-Like-1 (YKL-40) and Proinflammatory Biomarkers in the Pathogenesis of Pediatric Tick-Borne Encephalitis in a Polish Cohort.Journal of inflammation research · 2024Article
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- The critical role of interleukin-6 in protection against neurotropic flavivirus infection.Frontiers in cellular and infection microbiology · 2023Article
- Molecular pathogenesis of Japanese encephalitis and possible therapeutic strategies.Archives of virology · 2022Review
- Viral Safety Issues in the Production and Manufacturing of Human Immunoglobulin Preparations from Equine Plasma/Serum.Pharmaceutical chemistry journal · 2022Article
- Japanese Encephalitis Virus Infected Human Monocyte-Derived Dendritic Cells Activate a Transcriptional Network Leading to an Antiviral Inflammatory Response.Frontiers in immunology · 2021Article
- CCR2 Inhibition Reduces Neurotoxic Microglia Activation Phenotype After Japanese Encephalitis Viral Infection.Frontiers in cellular neuroscience · 2020Article
- Japanese encephalitis virus-induced neuropathology in mouse model infected through the conjunctival route.The Indian journal of medical research · 2019Article
- Review of Emerging Japanese Encephalitis Virus: New Aspects and Concepts about Entry into the Brain and Inter-Cellular Spreading.Pathogens (Basel, Switzerland) · 2019Review
- Host genetic control of mosquito-borne Flavivirus infections.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- CD8 T cells protect adult naive mice from JEV-induced morbidity via lytic function.PLoS neglected tropical diseases · 2017Article
- MicroRNA-based control of tick-borne flavivirus neuropathogenesis: Challenges and perspectives.Antiviral research · 2016Article
- A Single Amino Acid Substitution in the M Protein Attenuates Japanese Encephalitis Virus in Mammalian Hosts.Journal of virology · 2015Article
- A Japanese encephalitis virus genotype 5 molecular clone is highly neuropathogenic in a mouse model: impact of the structural protein region on virulence.Journal of virology · 2015Article
- Mice with different susceptibility to tick-borne encephalitis virus infection show selective neutralizing antibody response and inflammatory reaction in the central nervous system.Journal of neuroinflammation · 2013Article
- Biomarkers in Japanese encephalitis: a review.BioMed research international · 2013Review
- Protective immunity to Japanese encephalitis virus associated with anti-NS1 antibodies in a mouse model.Virology journal · 2012Article
- Encephalitis caused by flaviviruses.QJM : monthly journal of the Association of Physicians · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundJapanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes public health problems in Asian countries. Only a limited number of JEV-infected individuals show symptoms and develop severe encephalitis, indicating host-dependent susceptibilities. METHODOLOGY/PRINCIPAL
findingsC3H/HeN and DBA/2 mice, which exhibit different mortalities when infected by intraperitoneal inoculation with JEV, were used as experimental models to compare viral pathogenesis and host responses. One hundred infectious virus particles killed 95% of C3H/HeN mice whereas only 40% of DBA/2 mice died. JEV RNA was detected with similar low levels in peripheral lymphoid organs and in the sera of both mouse strains. High levels of viral and cytokine RNA were observed simultaneously in the brains of C3H/HeN and DBA/2 mice starting on days 6 and 9 post-infection, respectively. The kinetics of the cytokines in sera correlated with the viral replication in the brain. Significantly earlier and higher titers of neutralizing antibodies were detected in the DBA/2 strain. Primary embryonic fibroblasts, bone marrow-derived dendritic cells and macrophages from the two mouse strains were cultured. Fibroblasts displayed similar JEV replication abilities, whereas DBA/2-derived myeloid antigen-presenting cells had lower viral infectivity and production compared to the C3H/HeN-derived cells. CONCLUSIONS/SIGNIFICANCE: Mice with different susceptibilities to JEV neuroinvasion did not show changes in viral tropism and host innate immune responses prior to viral entry into the central nervous system. However, early and high neutralizing antibody responses may be crucial for preventing viral neuroinvasion and host fatality. In addition, low permissiveness of myeloid dendritic cells and macrophages to JEV infection in vitro may be elements associated with late and decreased mouse neuroinvasion.
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