Mouse hepatitis virus neurovirulence: evidence of a linkage between S glycoprotein expression and immunopathology.
Identifieur interne : 005233 ( Main/Exploration ); précédent : 005232; suivant : 005234Mouse hepatitis virus neurovirulence: evidence of a linkage between S glycoprotein expression and immunopathology.
Auteurs : Julia D. Rempel [États-Unis] ; Shannon J. Murray ; Jeffrey Meisner ; Michael J. BuchmeierSource :
- Virology [ 0042-6822 ] ; 2004.
Descripteurs français
- KwdFr :
- Animaux, Chimiokine CCL3, Chimiokine CCL4, Cytométrie en flux, Encéphale (cytologie), Encéphale (immunologie), Encéphale (virologie), Encéphalite virale (immunologie), Encéphalite virale (physiopathologie), Encéphalite virale (virologie), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (métabolisme), Infections à coronavirus (immunologie), Infections à coronavirus (physiopathologie), Infections à coronavirus (virologie), Lymphocytes T CD8+ (immunologie), Macrophages (virologie), Mâle, Protéines de l'enveloppe virale (métabolisme), Protéines inflammatoires des macrophages (métabolisme), Souris, Souris de lignée C57BL, Virulence, Virus de l'hépatite murine (génétique), Virus de l'hépatite murine (pathogénicité).
- MESH :
- cytologie : Encéphale.
- génétique : Virus de l'hépatite murine.
- immunologie : Encéphale, Encéphalite virale, Infections à coronavirus, Lymphocytes T CD8+.
- métabolisme : Glycoprotéines membranaires, Protéines de l'enveloppe virale, Protéines inflammatoires des macrophages.
- pathogénicité : Virus de l'hépatite murine.
- physiopathologie : Encéphalite virale, Infections à coronavirus.
- virologie : Encéphale, Encéphalite virale, Infections à coronavirus, Macrophages.
- Animaux, Chimiokine CCL3, Chimiokine CCL4, Cytométrie en flux, Glycoprotéine de spicule des coronavirus, Mâle, Souris, Souris de lignée C57BL, Virulence.
English descriptors
- KwdEn :
- Animals, Brain (cytology), Brain (immunology), Brain (virology), CD8-Positive T-Lymphocytes (immunology), Chemokine CCL3, Chemokine CCL4, Coronavirus Infections (immunology), Coronavirus Infections (physiopathology), Coronavirus Infections (virology), Encephalitis, Viral (immunology), Encephalitis, Viral (physiopathology), Encephalitis, Viral (virology), Flow Cytometry, Macrophage Inflammatory Proteins (metabolism), Macrophages (virology), Male, Membrane Glycoproteins (metabolism), Mice, Mice, Inbred C57BL, Murine hepatitis virus (genetics), Murine hepatitis virus (pathogenicity), Spike Glycoprotein, Coronavirus, Viral Envelope Proteins (metabolism), Virulence.
- MESH :
- chemical , metabolism : Macrophage Inflammatory Proteins, Membrane Glycoproteins, Viral Envelope Proteins.
- chemical : Chemokine CCL3, Chemokine CCL4, Spike Glycoprotein, Coronavirus.
- cytology : Brain.
- genetics : Murine hepatitis virus.
- immunology : Brain, CD8-Positive T-Lymphocytes, Coronavirus Infections, Encephalitis, Viral.
- pathogenicity : Murine hepatitis virus.
- physiopathology : Coronavirus Infections, Encephalitis, Viral.
- virology : Brain, Coronavirus Infections, Encephalitis, Viral, Macrophages.
- Animals, Flow Cytometry, Male, Mice, Mice, Inbred C57BL, Virulence.
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.
DOI: 10.1016/j.virol.2003.08.041
PubMed: 14972534
Affiliations:
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Le document en format XML
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coronavirus</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><noCountry><name sortKey="Buchmeier, Michael J" sort="Buchmeier, Michael J" uniqKey="Buchmeier M" first="Michael J" last="Buchmeier">Michael J. Buchmeier</name><name sortKey="Meisner, Jeffrey" sort="Meisner, Jeffrey" uniqKey="Meisner J" first="Jeffrey" last="Meisner">Jeffrey Meisner</name><name sortKey="Murray, Shannon J" sort="Murray, Shannon J" uniqKey="Murray S" first="Shannon J" last="Murray">Shannon J. Murray</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Rempel, Julia D" sort="Rempel, Julia D" uniqKey="Rempel J" first="Julia D" last="Rempel">Julia D. Rempel</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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