Previous Article | Next Article ![]()
Journal of Virology, December 2007, p. 13291-13298, Vol. 81, No. 24
0022-538X/07/$08.00+0 doi:10.1128/JVI.01580-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»