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and
Stanley Perlman1,2*
Program in Immunology,1 Department of Microbiology, University of Iowa; Iowa City, Iowa 522422
Received 19 July 2007/ Accepted 25 September 2007
Mutation within virus-derived CD8 T-cell epitopes can effectively abrogate cytotoxic T-lymphocyte (CTL) recognition and impede virus clearance in infected hosts. These so-called "CTL escape variant viruses" are commonly selected during persistent infections and are associated with rapid disease progression and increased disease severity. Herein, we tested whether antiviral antibody-mediated suppression of virus replication and subsequent virus clearance were necessary for preventing CTL escape in coronavirus-infected mice. We found that compared to wild-type mice, B-cell-deficient mice did not efficiently clear infectious virus, uniformly developed clinical disease, and harbored CTL escape variant viruses. These data directly demonstrate a critical role for antiviral antibody in protecting from the selective outgrowth of CTL escape variant viruses.
Published ahead of print on 3 October 2007.
Present address: Department of Internal Medicine, University of Washington, Seattle, WA 98195.
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
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| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
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