ArticleJournal of virology2006
CD8+ T cells require perforin to clear West Nile virus from infected neurons.
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 139 papers.
What it found
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The trial behind it
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
139 citing papers in PubMed, 215 citations in OpenAlex.
- IL-1β signaling promotes CNS-intrinsic immune control of West Nile virus infection.PLoS pathogens · 2012Trial
- Development of antigen-specific memory CD8+ T cells following live-attenuated chimeric West Nile virus vaccination.The Journal of infectious diseases · 2011Trial
- Multiple orthoflaviviruses secrete sfRNA in mosquito saliva to promote transmission by inhibiting MDA5-mediated early interferon response.Nature communications · 2026Article
- Brain endothelial cells orchestrate a neuroprotective antiviral state in the CNS in response to peripheral viral pattern sensing.Immunity · 2026Article
- Brain-infiltrating CD8 T cells retain functional activity to protect against acute Zika virus infection.Scientific reports · 2026Article
- MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8Journal of neuroinflammation · 2025Article
- Interleukin-17A signaling promotes CD8+ T cell cytotoxicity against West Nile virus infection through enhancing PI3K-mTOR-mediated metabolism.PLoS pathogens · 2025Article
- Review
- West Nile virus triggers intestinal dysmotility via T cell-mediated enteric nervous system injury.The Journal of clinical investigation · 2024Article
- Antigen non-specific CD8bioRxiv : the preprint server for biology · 2024Article
- A Pocket Guide to CCR5-Neurotropic Flavivirus Edition.Viruses · 2023Review
- Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections.Viruses · 2023Review
- Potential of Interleukin (IL)-12 Group as Antivirals: Severe Viral Disease Prevention and Management.International journal of molecular sciences · 2023Review
- Clodronate is not protective in lethal viral encephalitis despite substantially reducing inflammatory monocyte infiltration in the CNS.Frontiers in immunology · 2023Article
- The role of antiviral CD8Current opinion in neurobiology · 2022Review
- Single-cell RNA transcriptome analysis of CNS immune cells reveals CXCL16/CXCR6 as maintenance factors for tissue-resident T cells that drive synapse elimination.Genome medicine · 2022Article
- Lifelong cytomegalovirus and early-LIFE irradiation synergistically potentiate age-related defects in response to vaccination and infection.Aging cell · 2022Article
- MAVS mediates a protective immune response in the brain to Rift Valley fever virus.PLoS pathogens · 2022Article
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- Article
79 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
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Injury to neurons after West Nile virus (WNV) infection is believed to occur because of viral and host immune-mediated effects. Previously, we demonstrated that CD8+ T cells are required for the resolution of WNV infection in the central nervous system (CNS). CD8+ T cells can control infection by producing antiviral cytokines (e.g., gamma interferon or tumor necrosis factor alpha) or by triggering death of infected cells through perforin- or Fas ligand-dependent pathways. Here, we directly evaluated the role of perforin in controlling infection of a lineage I New York isolate of WNV in mice. A genetic deficiency of perforin molecules resulted in higher viral burden in the CNS and increased mortality after WNV infection. In the few perforin-deficient mice that survived initial challenge, viral persistence was observed in the CNS for several weeks. CD8+ T cells required perforin to control WNV infection as adoptive transfer of WNV-primed wild-type but not perforin-deficient CD8+ T cells greatly reduced infection in the brain and spinal cord and enhanced survival of CD8-deficient mice. Analogous results were obtained when wild-type or perforin-deficient CD8+ T cells were added to congenic primary cortical neuron cultures. Taken together, our data suggest that despite the risk of immunopathogenesis, CD8+ T cells use a perforin-dependent mechanism to clear WNV from infected neurons.
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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.