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PMID: 10666278 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Contributions of Fas-Fas ligand interactions to the pathogenesis of mouse hepatitis virus in the central nervous system.

Journal of virology ·Vol. 74 ·No. 5 ·2000-03-00 ·Pages 2447-50

Parra B, Lin MT, Stohlman SA, Bergmann CC, Atkinson R, Hinton DR

Abstract

The pathogenesis of the neurotropic strain of mouse hepatitis virus in Fas-deficient mice suggested that Fas-mediated cytotoxicity may be required during viral clearance after the loss of perforin-mediated cytotoxicity. The absence of both Fas- and perforin-mediated cytolysis resulted in an uncontrolled infection, suggesting a redundancy of cytolytic pathways to control virus replication.

MeSH Terms
Animals Brain/pathology,virology Cell Line Central Nervous System Infections/pathology,virology Coronavirus Infections/pathology,virology Fas Ligand Protein Membrane Glycoproteins/genetics,immunology Mice Mice, Inbred C57BL Mice, Knockout Murine hepatitis virus/pathogenicity Perforin Pore Forming Cytotoxic Proteins Spinal Cord/pathology fas Receptor/genetics,immunology
Chemicals
Fas Ligand Protein Fasl protein, mouse Membrane Glycoproteins Pore Forming Cytotoxic Proteins fas Receptor Perforin
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Parra B
Departments of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.
Lin M T
Stohlman S A
Bergmann C C
Atkinson R
Hinton D R
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
DOI
10.1128/jvi.74.5.2447-2450.2000
Published
2000-03-00
Pages
2447-50
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC111729
Subset
IM
Grants
NINDS NIH HHS · P01 NS018146 · United States
NINDS NIH HHS · NS 18146 · United States
External Links
PubMed source DOI: 10.1128/jvi.74.5.2447-2450.2000 PMC Full Text View journal details
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