ArticleJournal of virology2010
The innate immune adaptor molecule MyD88 restricts West Nile virus replication and spread in neurons of the central nervous system.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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
89 citing papers in PubMed, 107 citations in OpenAlex.
- IL-1β signaling promotes CNS-intrinsic immune control of West Nile virus infection.PLoS pathogens · 2012Trial
- Neutrophils repurpose the nucleolus as a cytokine reservoir and secretory organelle.bioRxiv : the preprint server for biology · 2026Article
- MyD88 signaling in myeloid cells induces gastrointestinal tract injury and systemic inflammation after West Nile virus infection.Cell reports · 2026Article
- Opportunities and Challenges of mRNA and VLP Technologies for Pan-Flavivirus Vaccine Development: Focus on Conserved Quaternary Epitope Conformations.International journal of molecular sciences · 2026Review
- The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.Journal of virology · 2025Article
- Comparison of innate immune responses against arboviruses in mammalian hosts and mosquito vectors.hLife · 2025Review
- cGAS/STING-Independent Induction of Type I Interferon by Inhibitors of the Histone Methylase KDM5B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Innate immune sensing and vaccine strategies against West Nile virus: role of Toll-like receptors and viral evasion mechanisms.Frontiers in microbiology · 2025Review
- Article
- Orchestration of antiviral responses within the infected central nervous system.Cellular & molecular immunology · 2024Review
- Inhibition of NADPH oxidase 2 enhances resistance to viral neuroinflammation by facilitating M1-polarization of macrophages at the extraneural tissues.Journal of neuroinflammation · 2024Article
- RIPK3 promotes brain region-specific interferon signaling and restriction of tick-borne flavivirus infection.PLoS pathogens · 2023Article
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- The MAVS Immune Recognition Pathway in Viral Infection and Sepsis.Antioxidants & redox signaling · 2021Review
- Toll-like Receptors in Viral Encephalitis.Viruses · 2021Review
- Genetic targeting of Card19 is linked to disrupted NINJ1 expression, impaired cell lysis, and increased susceptibility to Yersinia infection.PLoS pathogens · 2021Article
- MyD88 signaling by neurons induces chemokines that recruit protective leukocytes to the virus-infected CNS.Science immunology · 2021Article
- Review
- Unique Cytokine Response in West Nile Virus Patients Who Developed Chronic Kidney Disease: A Prospective Cohort Study.Viruses · 2021Article
- Host genetic susceptibility to viral infections: the role of type I interferon induction.Genes and immunity · 2020Review
29 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
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Type I interferons (IFN-α/β) control viral infection by triggering the expression of genes that restrict transcription, translation, replication, and assembly. Many viruses induce IFN responses after recognition by cytoplasmic or endosomal RNA sensors (RIG-I-like RNA helicases [RLR] and Toll-like receptors [TLR]), which signal through the cognate adaptor signaling molecules IPS-1, TRIF, and MyD88. Recent studies have demonstrated that IPS-1-dependent induction of IFN-α/β downstream of RLR recognition restricts West Nile virus (WNV) infection in many cell types, whereas TRIF-dependent TLR3 signaling limits WNV replication in neurons. Here, we examined the contribution of MyD88 signaling to the control of WNV by evaluating IFN induction and virus replication in genetically deficient cells and mice. MyD88(-/-) mice showed increased lethality after WNV infection and elevated viral burden primarily in the brain, even though little effect on the systemic type I IFN response was observed. Intracranial inoculation studies corroborated these findings, as WNV spread more rapidly in the central nervous system of MyD88(-/-) mice, and this phenotype preceded the recruitment of inflammatory leukocytes. In vitro, increased WNV replication was observed in MyD88(-/-) macrophages and subsets of neurons but not in myeloid dendritic cells. MyD88 had an independent effect on recruitment of monocyte-derived macrophages and T cells into the brain that was associated with blunted induction of the chemokines that attract leukocytes. Our experiments suggest that MyD88 restricts WNV by inhibiting replication in subsets of cells and modulating expression of chemokines that regulate immune cell migration into the central nervous system.
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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.