Contributions of Fas-Fas ligand interactions to the pathogenesis of mouse hepatitis virus in the central nervous system.
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.
Parra
B
B
Departments of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA.
Lin
M T
MT
Stohlman
S A
SA
Bergmann
C C
CC
Atkinson
R
R
Hinton
D R
DR
D000818:Animals; D001921:Brain / Q000473:pathology / Q000821:virology; D002460:Cell Line; D002494:Central Nervous System Infections / Q000473:pathology / Q000821:virology*; D018352:Coronavirus Infections / Q000473:pathology / Q000821:virology*; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D006517:Murine hepatitis virus / Q000472:pathogenicity*; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D013116:Spinal Cord / Q000473:pathology; D019014:fas Receptor / Q000235:genetics / Q000276:immunology*
D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D019014:fas Receptor; D054353:Perforin