ArticlePloS one2012
The chemokine receptor CCR5, a therapeutic target for HIV/AIDS antagonists, is critical for recovery in a mouse model of Japanese encephalitis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- A Xeno-Free Protocol for Rapid Differentiation of Human iPSC-Derived Microglia from the KOLF2.1J Reference Line.Bioengineering (Basel, Switzerland) · 2025Article
- A xeno-free protocol for rapid differentiation of human iPSC-derived microglia from the KOLF2.1J reference line.bioRxiv : the preprint server for biology · 2025Article
- CXCR4 and CXCR6 dually limit T cell entry into the polyomavirus-infected brain.Journal of neuroinflammation · 2025Article
- Usutu virus-induced meningoencephalitis in immunocompetent mice is characterized by the recruitment of mononuclear cells and a proinflammatory T helper 1 response.Journal of virology · 2025Article
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- A Pocket Guide to CCR5-Neurotropic Flavivirus Edition.Viruses · 2023Review
- Neuroinvasive Flavivirus Pathogenesis Is Restricted by Host Genetic Factors in Collaborative Cross Mice, Independently ofJournal of virology · 2023Article
- Genomics and epigenetics guided identification of tissue-specific genomic safe harbors.Genome biology · 2022Article
- The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population.Pathogens (Basel, Switzerland) · 2022Article
- Powassan Viruses Spread Cell to Cell during Direct Isolation fromJournal of virology · 2022Article
- CCR5 antagonist treatment inhibits vascular injury by regulating NADPH oxidase 1.Biochemical pharmacology · 2022Article
- Article
- Landscape of Preterm Birth Therapeutics and a Path Forward.Journal of clinical medicine · 2021Review
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Chemokine Profile and the Alterations in CCR5-CCL5 Axis in Geographic Atrophy Secondary to Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2020Observational
- Targeted Gene Delivery: Where to Land.Frontiers in genome editing · 2020Review
- PD1Virologica Sinica · 2019Article
- A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection.BMC evolutionary biology · 2017Article
- Regulation of inflammation in Japanese encephalitis.Journal of neuroinflammation · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis is a severe central nervous system (CNS) inflammatory disease caused by the mosquito-borne flavivirus, Japanese encephalitis virus (JEV). In the current study we have investigated the immune responses against JEV in mice lacking expression of the chemokine receptor CCR5, which functions in activation and chemotaxis of leukocytes during infection. We show that CCR5 serves as a host antiviral factor against Japanese encephalitis, with CCR5 deficiency markedly increasing mortality, and viral burden in the CNS. Humoral immune responses, which are essential in recovery from JEV infection, were of similar magnitude in CCR5 sufficient and deficient mice. However, absence of CCR5 resulted in a multifaceted deficiency of cellular immune responses characterized by reduced natural killer and CD8⁺ T cell activity, low splenic cellularity, and impaired trafficking of leukocytes to the brain. Interestingly, adoptive transfer of immune spleen cells, depleted of B lymphocytes, increased resistance of CCR5-deficient recipient mice against JEV regardless of whether the cells were obtained from CCR5-deficient or wild-type donor mice, and only when transferred at one but not at three days post-challenge. This result is consistent with a mechanism by which CCR5 expression enhances lymphocyte activation and thereby promotes host survival in Japanese encephalitis.
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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.