ArticleVirology2004
Mouse hepatitis virus neurovirulence: evidence of a linkage between S glycoprotein expression and immunopathology.
Article in Virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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
25 citing papers in PubMed.
- Article
- Insights into coronavirus immunity taught by the murine coronavirus.European journal of immunology · 2021Review
- Neurological Complications of COVID-19: Underlying Mechanisms and Management.International journal of molecular sciences · 2021Review
- Of Mice and Men: The Coronavirus MHV and Mouse Models as a Translational Approach to Understand SARS-CoV-2.Viruses · 2020Review
- Murine coronavirus neuropathogenesis: determinants of virulence.Journal of neurovirology · 2010Review
- Pathogenesis of murine coronavirus in the central nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Review
- Murine coronavirus delays expression of a subset of interferon-stimulated genes.Journal of virology · 2010Article
- Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response.Viruses · 2009Article
- Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.Microbiology and molecular biology reviews : MMBR · 2008Review
- Murine coronavirus mouse hepatitis virus is recognized by MDA5 and induces type I interferon in brain macrophages/microglia.Journal of virology · 2008Article
- CXCR4 antagonism increases T cell trafficking in the central nervous system and improves survival from West Nile virus encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Priming of CD8+ T cells during central nervous system infection with a murine coronavirus is strain dependent.Journal of virology · 2008Article
- Chemokine expression during mouse-hepatitis-virus-induced encephalitis: contributions of the spike and background genes.Journal of neurovirology · 2008Article
- The spike glycoprotein of murine coronavirus MHV-JHM mediates receptor-independent infection and spread in the central nervous systems of Ceacam1a-/- Mice.Journal of virology · 2008Article
- The coronavirus spike protein induces endoplasmic reticulum stress and upregulation of intracellular chemokine mRNA concentrations.Journal of virology · 2007Article
- Inhibition of the alpha/beta interferon response by mouse hepatitis virus at multiple levels.Journal of virology · 2007Article
- A hypervariable region within the 3' cis-acting element of the murine coronavirus genome is nonessential for RNA synthesis but affects pathogenesis.Journal of virology · 2007Article
- Pathogenesis of acute and chronic central nervous system infection with variants of mouse hepatitis virus, strain JHM.Immunologic research · 2007Review
- Both spike and background genes contribute to murine coronavirus neurovirulence.Journal of virology · 2006Article
- Coronavirus infection of the central nervous system: host-virus stand-off.Nature reviews. Microbiology · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Differences in disease outcome between the highly neurovirulent MHV-JHM and mildly neurovirulent MHV-A59 have been attributed to variations within the spike (S) glycoprotein. Previously, we found that MHV-JHM neurovirulence was marked by diminished expression of interferon-gamma (IFN-gamma) mRNA and a reduced presence of CD8 T cells in the CNS concomitant with heightened macrophage inflammatory protein (MIP)-1 transcript levels and greater macrophage infiltration relative to MHV-A59 infection. Here, the ability of the S and non-spike genes to regulate these immune responses was evaluated using chimeric viruses. Chimeric viruses WTR13 and S4R22 were made on MHV-A59 variant backgrounds and, respectively, contained the S gene of MHV-A59 and MHV-JHM. Unexpectedly, genes other than S appeared to modulate events critical to viral replication and survival. Unlike unresolving MHV-JHM infections, the clearance of WTR13 and S4R22 infections coincided with strong IFN-gamma transcription and an increase in the number of CD8 T cells infiltrating into the CNS. However, despite the absence of detectable viral titers, approximately 40% of S4R22-infected mice succumbed within 3 weeks, indicating that the enhanced mortality following S4R22 infection was not associated with high viral titers. Instead, similar to the MHV-JHM infection, reduced survival following S4R22 infection was observed in the presence of elevated MIP-1alpha and MIP-1beta mRNA accumulation and enhanced macrophage numbers within infected brains. These observations suggest that the S protein of MHV-JHM influences neurovirulence through the induction of MIP-1alpha- and MIP-1beta-driven macrophage immunopathology.
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