ArticleProceedings of the National Academy of Sciences of the United States of America2002
A nonsense mutation in the gene encoding 2'-5'-oligoadenylate synthetase/L1 isoform is associated with West Nile virus susceptibility in laboratory mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 2 of them syntheses that pooled it.
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Who cites it
122 citing papers in PubMed, 2 syntheses or guidelines pooled it, 275 citations in OpenAlex.
- Correlation Between West Nile Virus and Pregnancy: A Systematic Review.Pathogens (Basel, Switzerland) · 2024Pooled it
- Identification of genetic variants associated with dengue or West Nile virus disease: a systematic review and meta-analysis.BMC infectious diseases · 2018Pooled it
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- Article
- The OAS-RNase L pathway: Insights from experiments of nature.Science immunology · 2026Review
- The canonical antiviral protein oligoadenylate synthetase 1 elicits antibacterial functions by enhancing IRF1 translation.Immunity · 2024Article
- Functional Analysis of Oligoadenylate Synthetase in the Emu (Animals : an open access journal from MDPI · 2024Article
- Oligoadenylate synthetase 1 displays dual antiviral mechanisms in driving translational shutdown and protecting interferon production.Immunity · 2024Article
- Host Genetic Variation Has a Profound Impact on Immune Responses Mediating Control of Viral Load in Chronic Gammaherpesvirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The Many Faces of Oligoadenylate Synthetases.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Review
- Neuroinvasive Flavivirus Pathogenesis Is Restricted by Host Genetic Factors in Collaborative Cross Mice, Independently ofJournal of virology · 2023Article
- Specific Recognition of the 5'-Untranslated Region of West Nile Virus Genome by Human Innate Immune System.Viruses · 2022Article
- IncreasedViruses · 2022Article
- Activation of the antiviral factor RNase L triggers translation of non-coding mRNA sequences.Nucleic acids research · 2021Article
- The Restrictome of Flaviviruses.Virologica Sinica · 2020Review
- Review
- 2', 5'-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway.Viruses · 2020Article
- Genetic Diversity of Collaborative Cross Mice Controls Viral Replication, Clinical Severity, and Brain Pathology Induced by Zika Virus Infection, Independently ofJournal of virology · 2020Article
- Comparative Pathology of West Nile Virus in Humans and Non-Human Animals.Pathogens (Basel, Switzerland) · 2020Review
- Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A mouse model has been established to investigate the genetic determinism of host susceptibility to West Nile (WN) virus, a member of the genus flavivirus and family Flaviviridae. Whereas WN virus causes encephalitis and death in most laboratory inbred mouse strains after peripheral inoculation, most strains derived from recently trapped wild mice are completely resistant. The phenotype of resistance/susceptibility is determined by a major locus, Wnv, mapping to chromosome 5 within the 0.4-cM-wide interval defined by markers D5Mit408 and D5Mit242. We constructed a high resolution composite/consensus map of the interval by merging the data from the mouse T31 Radiation Hybrid map and those from the homologous region of human chromosome 12q, and found the cluster of genes encoding 2'-5'-oligoadenylate synthetases (2'-5'-OAS) to be the most prominent candidate. This cluster encodes a multimember family of IFN-inducible proteins that is known to play an important role in the established endogenous antiviral pathway. Comparing the cDNA sequences of 2'-5'-OAS L1, L2, and L3 isoforms, between susceptible and resistant strains, we identified a STOP codon in exon 4 of the gene encoding the L1 isoform in susceptible strains that can lead to a truncated form with amputation of one domain, whereas all resistant mice tested so far have a normal copy of this gene. The observation that WN virus sensitivity of susceptible mice was completely correlated with the occurrence of a point mutation in 2'-5'-OAS L1 suggests that this isoform may play a critical role in WN pathogenesis.
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