JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.01848-07v1
82/3/1314    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Okeoma, C. M.
Right arrow Articles by Ross, S. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Okeoma, C. M.
Right arrow Articles by Ross, S. R.

 Previous Article  |  Next Article 

Journal of Virology, February 2008, p. 1314-1322, Vol. 82, No. 3
0022-538X/08/$08.00+0     doi:10.1128/JVI.01848-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Novel Block to Mouse Mammary Tumor Virus Infection of Lymphocytes in B10.BR Mice{triangledown}

Chioma M. Okeoma, Ming Shen, and Susan R. Ross*

Department of Microbiology and Abramson Family Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Received 22 August 2007/ Accepted 1 November 2007

Classic studies on C57BL-derived mouse strains showed that they were resistant to mouse mammary tumor virus (MMTV) infection. Although one form of resistance mapped to the major histocompatibility complex (MHC) locus, at least one other, unknown gene was implicated in this resistance. We show here that B10.BR mice, which are derived from C57BL mice but have the same MHC locus (H-2k) as susceptible C3H/HeN mice, are resistant to MMTV, and show a lack of virus spread in their lymphoid compartments but not their mammary epithelial cells. Although in vivo virus superantigen (Sag)-mediated activation of T cells was similar in C3H/HeN and B10.BR mice, T cell-dependent B-cell and dendritic cell activation was diminished in the latter. Ex vivo, B10.BR T cells showed a diminished capacity to proliferate in response to the MMTV Sag. The genetic segregation of the resistance phenotype indicated that it maps to a single allele. These data highlight the role of Sag-dependent T-cell responses in MMTV infection and point to a novel mechanism for the resistance of mice to retroviral infection that could lead to a better understanding of the interplay between hosts and pathogens.

* Corresponding author. Mailing address: Room 313 BRBII/III, University of Pennsylvania, 421 Curie Blvd., Philadelphia, PA 19104-6142. Phone: (215) 898-9764. Fax: (215) 573-2028. E-mail: rosss{at}mail.med.upenn.edu

{triangledown} Published ahead of print on 14 November 2007.

Journal of Virology, February 2008, p. 1314-1322, Vol. 82, No. 3
0022-538X/08/$08.00+0     doi:10.1128/JVI.01848-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2008 by the American Society for Microbiology. All rights reserved.