Logo image
Role of CTL Mutants in Demyelination Induced by Mouse Hepatitis Virus, Strain JHM
Journal article   Open access   Peer reviewed

Role of CTL Mutants in Demyelination Induced by Mouse Hepatitis Virus, Strain JHM

S Perlman and L Pewe
Advances in experimental medicine and biology, Vol.440, pp.515-519
1998
DOI: 10.1007/978-1-4615-5331-1_66.
PMID: 9782323
url
https://doi.org/10.1007/978-1-4615-5331-1_66.View
Published (Version of record) Open Access

Abstract

Mouse hepatitis virus, strain JHM (MHV-JHM) is a well described cause of demyelination. C57B1/6 (B6) mice infected at the suckling stage in the presence of protective antibodies remain asymptomatic initially but later develop clinical disease (hindlimb paralysis). Infectious virus can be isolated from these mice. Recently, two MHV-specific target epitopes for cytotoxic CD8 T cells have been identified in B6 mice. Our results show that in all mice with hindlimb paralysis, mutations can be detected in the RNA encoding the immunodominant of the two epitopes. These mutations result in a loss of recognition by MHV-specific cytotoxic T cells. These changes are not detected, for the most part, in mice that remain asymptomatic nor in mice with acute encephalitis. These results suggest that the development of CTL escape mutants is necessary for hindlimb paralysis to develop in this model.
Mutation Murine hepatitis virus - immunology T-Lymphocytes, Cytotoxic - immunology Animals Demyelinating Diseases - virology Demyelinating Diseases - immunology Coronavirus Infections - complications Mice Murine hepatitis virus - pathogenicity Coronavirus Infections - immunology

Details

Metrics

Logo image