ArticlePLoS pathogens2009
RNase L mediated protection from virus induced demyelination.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- POTENTIAL RISK OF BRAIN DAMAGE AND POOR DEVELOPMENTAL OUTCOMES IN CHILDREN PRENATALLY EXPOSED TO SARS-COV-2: A SYSTEMATIC REVIEW.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2021Pooled it
- tRNA modifications in viral replication.The Journal of biological chemistry · 2026Review
- The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.Viruses · 2023Review
- A Potential Association between Ribonuclease 1 Dynamics in the Blood and the Outcome in COVID-19 Patients.International journal of molecular sciences · 2023Article
- Host Defence RNases as Antiviral Agents against Enveloped Single Stranded RNA Viruses.Virulence · 2021Review
- Activation of the antiviral factor RNase L triggers translation of non-coding mRNA sequences.Nucleic acids research · 2021Article
- SARS-CoV-2 and other human coronavirus show genome patterns previously associated to reduced viral recognition and altered immune response.Scientific reports · 2021Article
- Expression of Human ACE2 N-terminal Domain, Part of the Receptor for SARS-CoV-2, in Fusion With Maltose-Binding Protein,Frontiers in microbiology · 2021Article
- tRNA-derived fragments and microRNAs in the maternal-fetal interface of a mouse maternal-immune-activation autism model.RNA biology · 2020Article
- Review
- Article
- Real-time 2-5A kinetics suggest that interferons β and λ evade global arrest of translation by RNase L.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Dom34 mediates targeting of exogenous RNA in the antiviral OAS/RNase L pathway.Nucleic acids research · 2019Article
- Rapid RNase L-driven arrest of protein synthesis in the dsRNA response without degradation of translation machinery.RNA (New York, N.Y.) · 2017Article
- RNase L Suppresses Androgen Receptor Signaling, Cell Migration and Matrix Metalloproteinase Activity in Prostate Cancer Cells.International journal of molecular sciences · 2017Article
- CXCL13 promotes isotype-switched B cell accumulation to the central nervous system during viral encephalomyelitis.Brain, behavior, and immunity · 2016Article
- The Roles of RNase-L in Antimicrobial Immunity and the Cytoskeleton-Associated Innate Response.International journal of molecular sciences · 2016Review
- Myd88 Initiates Early Innate Immune Responses and Promotes CD4 T Cells during Coronavirus Encephalomyelitis.Journal of virology · 2015Article
- Enzymatic Pre-treatment of Wastewater to Minimize Recovery by Reverse Transcriptase PCR of RNA from Inactive Bacteriophages.Current microbiology · 2015Article
- Progression from IgD+ IgM+ to isotype-switched B cells is site specific during coronavirus-induced encephalomyelitis.Journal of virology · 2014Article
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 1 country.
Funding
Abstract
IFN-alpha/beta plays a critical role in limiting viral spread, restricting viral tropism and protecting mice from neurotropic coronavirus infection. However, the IFN-alpha/beta dependent mechanisms underlying innate anti-viral functions within the CNS are poorly understood. The role of RNase L in viral encephalomyelitis was explored based on its functions in inhibiting translation, inducing apoptosis, and propagating the IFN-alpha/beta pathway through RNA degradation intermediates. Infection of RNase L deficient (RL(-/-)) mice with a sub-lethal, demyelinating mouse hepatitis virus variant revealed that the majority of mice succumbed to infection by day 12 p.i. However, RNase L deficiency did not affect overall control of infectious virus, or diminish IFN-alpha/beta expression in the CNS. Furthermore, increased morbidity and mortality could not be attributed to altered proinflammatory signals or composition of cells infiltrating the CNS. The unique phenotype of infected RL(-/-) mice was rather manifested in earlier onset and increased severity of demyelination and axonal damage in brain stem and spinal cord without evidence for enhanced neuronal infection. Increased tissue damage coincided with sustained brain stem infection, foci of microglia infection in grey matter, and increased apoptotic cells. These data demonstrate a novel protective role for RNase L in viral induced CNS encephalomyelitis, which is not reflected in overall viral control or propagation of IFN-alpha/beta mediated signals. Protective function is rather associated with cell type specific and regional restriction of viral replication in grey matter and ameliorated neurodegeneration and demyelination.
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What OpenQuestion holds
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.