ArticleJournal of virology2006
CD4+ T-cell responses are required for clearance of West Nile virus from the central nervous system.
Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
149 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-analysis of all immune epitope data in the Flavivirus genus: inventory of current immune epitope data status in the context of virus immunity and immunopathology.Viral immunology · 2010Pooled it
- West Nile Virus in People with HIV: Immune Vulnerability, Neuroinvasive Disease, and Diagnostic Challenges.Tropical medicine and infectious disease · 2026Review
- Cross-protection against St. Louis encephalitis virus and Usutu virus by West Nile virus convalescent plasma.Virology · 2025Article
- Cross-Protection between West Nile Virus and Emerging Flaviviruses in Wild Birds.The American journal of tropical medicine and hygiene · 2025Article
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
- West Nile virus triggers intestinal dysmotility via T cell-mediated enteric nervous system injury.The Journal of clinical investigation · 2024Article
- Impact of the microbiome on mosquito-borne diseases.Protein & cell · 2023Review
- Article
- Methods to Study West Nile Virus Infection and the Virus-Induced Inflammation in the Brain in a Murine Model.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Clodronate is not protective in lethal viral encephalitis despite substantially reducing inflammatory monocyte infiltration in the CNS.Frontiers in immunology · 2023Article
- The difference in CD4Frontiers in immunology · 2022Article
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- Article
- Intrinsic Innate Immune Responses Control Viral Growth and Protect against Neuronal Death in anJournal of virology · 2021Article
- Article
- Pathogenesis of Two Western Mediterranean West Nile Virus Lineage 1 Isolates in Experimentally Infected Red-Legged Partridges (Pathogens (Basel, Switzerland) · 2021Article
- Antiviral Cytokine Response in Neuroinvasive and Non-Neuroinvasive West Nile Virus Infection.Viruses · 2021Article
- A genetically stable Zika virus vaccine candidate protects mice against virus infection and vertical transmission.NPJ vaccines · 2021Article
- Neuroprotective versus Neuroinflammatory Roles of Complement: From Development to Disease.Trends in neurosciences · 2021Review
- The roles of microglia in viral encephalitis: from sensome to therapeutic targeting.Cellular & molecular immunology · 2021Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Although studies have established that innate and adaptive immune responses are important in controlling West Nile virus (WNV) infection, the function of CD4(+) T lymphocytes in modulating viral pathogenesis is less well characterized. Using a mouse model, we examined the role of CD4(+) T cells in coordinating protection against WNV infection. A genetic or acquired deficiency of CD4(+) T cells resulted in a protracted WNV infection in the central nervous system (CNS) that culminated in uniform lethality by 50 days after infection. Mice surviving past day 10 had high-level persistent WNV infection in the CNS compared to wild-type mice, even 45 days following infection. The absence of CD4(+) T-cell help did not affect the kinetics of WNV infection in the spleen and serum, suggesting a role for CD4-independent clearance mechanisms in peripheral tissues. WNV-specific immunoglobulin M (IgM) levels were similar to those of wild-type mice in CD4-deficient mice early during infection but dropped approximately 20-fold at day 15 postinfection, whereas IgG levels in CD4-deficient mice were approximately 100- to 1,000-fold lower than in wild-type mice throughout the course of infection. WNV-specific CD8(+) T-cell activation and trafficking to the CNS were unaffected by the absence of CD4(+) T cells at day 9 postinfection but were markedly compromised at day 15. Our experiments suggest that the dominant protective role of CD4(+) T cells during primary WNV infection is to provide help for antibody responses and sustain WNV-specific CD8(+) T-cell responses in the CNS that enable viral clearance.
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Registered trials
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.