Journal article
Protection against CTL escape and clinical disease in a murine model of virus persistence
Journal of immunology (Baltimore, Md. : 1950), Vol.171(4), pp.2006-2013
08/15/2003
DOI: 10.4049/jimmunol.171.4.2006
PMID: 12902505
Abstract
CTL escape mutations have been identified in several chronic infections, including mice infected with mouse hepatitis virus strain JHM. One outstanding question in understanding CTL escape is whether a CD8 T cell response to two or more immunodominant CTL epitopes would prevent CTL escape. Although CTL escape at multiple epitopes seems intuitively unlikely, CTL escape at multiple CD8 T cell epitopes has been documented in some chronically infected individual animals. To resolve this apparent contradiction, we engineered a recombinant variant of JHM that expressed the well-characterized gp33 epitope of lymphocytic choriomeningitis virus, an epitope with high functional avidity. The results show that the presence of a host response to this second epitope protected mice against CTL escape at the immunodominant JHM-specific CD8 T cell epitope, the persistence of infectious virus, and the development of clinical disease.
Details
- Title: Subtitle
- Protection against CTL escape and clinical disease in a murine model of virus persistence
- Creators
- Taeg S Kim - Interdisciplinary Program in Immunology, Department of Pediatrics, University of Iowa, Iowa City, IA 52242, USAStanley Perlman
- Resource Type
- Journal article
- Publication Details
- Journal of immunology (Baltimore, Md. : 1950), Vol.171(4), pp.2006-2013
- DOI
- 10.4049/jimmunol.171.4.2006
- PMID
- 12902505
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Publisher
- United States
- Grant note
- NS36592 / NINDS NIH HHS
- Language
- English
- Date published
- 08/15/2003
- Academic Unit
- Microbiology and Immunology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Infectious Disease (Pediatrics)
- Record Identifier
- 9983777469502771
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