ArticleJournal of neurovirology2007
Peripheral, but not central nervous system, type I interferon expression in mice in response to intranasal vesicular stomatitis virus infection.
Article in Journal of neurovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Olfactory immunity: defending the neural-mucosal barrier.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Viral infections of the central nervous system increase the risk of knee osteoarthritis: a two-sample mendelian randomization study.Aging clinical and experimental research · 2025Article
- Olfactory immunology: the missing piece in airway and CNS defence.Nature reviews. Immunology · 2024Review
- Antiviral Functions of Type I and Type III Interferons in the Olfactory Epithelium.Biomolecules · 2023Article
- Expression and mechanisms of interferon-stimulated genes in viral infection of the central nervous system (CNS) and neurological diseases.Frontiers in immunology · 2022Review
- A critical role for MSR1 in vesicular stomatitis virus infection of the central nervous system.iScience · 2021Article
- Rhabdoviruses as vectors for vaccines and therapeutics.Current opinion in virology · 2020Review
- The VSV matrix protein inhibits NF-κB and the interferon response independently in mouse L929 cells.Virology · 2020Article
- Experimental Evolution Generates Novel Oncolytic Vesicular Stomatitis Viruses with Improved Replication in Virus-Resistant Pancreatic Cancer Cells.Journal of virology · 2020Article
- The brain parenchyma has a type I interferon response that can limit virus spread.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Nuclear receptor REV-ERBα mediates circadian sensitivity to mortality in murine vesicular stomatitis virus-induced encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Oncolytic vesicular stomatitis virus expressing interferon-γ has enhanced therapeutic activity.Molecular therapy oncolytics · 2016Article
- An unexpected inhibition of antiviral signaling by virus-encoded tumor suppressor p53 in pancreatic cancer cells.Virology · 2015Article
- Creation of matrix protein gene variants of two serotypes of vesicular stomatitis virus as prime-boost vaccine vectors.Journal of virology · 2015Article
- Changes in Susceptibility to Oncolytic Vesicular Stomatitis Virus during Progression of Prostate Cancer.Journal of virology · 2015Article
- Upon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis.Journal of virology · 2015Article
- Article
- Type III interferon attenuates a vesicular stomatitis virus-based vaccine vector.Journal of virology · 2014Article
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Long-distance interferon signaling within the brain blocks virus spread.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
3 authors at 2 institutions in 1 country.
Funding
Abstract
Type I interferon (IFN) is critical for resistance of mice to infection with vesicular stomatitis virus (VSV). Wild type (wt) VSV infection did not induce type I IFN production in vitro or in the central nervous system (CNS) of mice; however IFN-beta was detected in lungs, spleen, and serum within 24 h. The M protein mutant VSV, T1026R1 (also referred to as M51R), induced type I IFN production in vitro and in the CNS, with poor expression in spleens. In addition, VSV T1026R1 was not pathogenic to mice after intranasal infection, illustrating the importance of IFN in controlling VSV replication in the CNS. Experiments with chemical sympathectomy, sRAGE, and neutralizing antibody to VSV were performed to investigate the mechanism(s) utilized for induction of peripheral IFN; neither sRAGE infusion nor chemical sympathectomy had an effect on peripheral IFN production. In contrast, administration of neutralizing antibody (Ab) readily blocked the response. Infectious VSV was transiently present in lungs and spleens at 24 h post infection. The results are consistent with VSV traffic from the olfactory neuroepithelium to peripheral lymphoid organs hematogenously or via lymphatic circulation. These results suggest that VSV replicates to high titers in the brains of mice because of the lack of IFN production in the CNS after intranasal VSV infection. In contrast, replication of VSV in peripheral organs is controlled by the production of large amounts of IFN.
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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.