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 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 Obar, J. J.
Right arrow Articles by Usherwood, E. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Obar, J. J.
Right arrow Articles by Usherwood, E. J.

 Previous Article  |  Next Article 

Journal of Virology, October 2004, p. 10829-10832, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10829-10832.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

T-Cell Responses to the M3 Immune Evasion Protein of Murid Gammaherpesvirus 68 Are Partially Protective and Induced with Lytic Antigen Kinetics

Joshua J. Obar,1 Douglas C. Donovan,1,{dagger} Sarah G. Crist,1 Ondine Silvia,2 James P. Stewart,2,{ddagger} and Edward J. Usherwood1*

Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, New Hampshire,1 Department of Veterinary Pathology, University of Edinburgh, Edinburgh, United Kingdom2

Received 31 July 2003/ Accepted 24 June 2004

DNA vaccination with the M3 gene, encoding an immune evasion molecule expressed during both the acute lytic and persistent phases of murid gammaherpesvirus 68 infection, yielded a significantly lower titer of virus in the lung than controls. The protection seen was dependent on T cells, and we mapped an epitope recognized by CD8 T cells. The immune response to this epitope follows the same kinetics as lytic cycle antigens, despite the fact that this gene is expressed in both lytic and persistent stages of infection. This has important implications for our understanding of T-cell responses to putative latency-associated gammaherpesvirus proteins and how vaccination may improve control of these viruses.


* Corresponding author. Mailing address: Department of Microbiology and Immunology, 608E Borwell Building, 1 Medical Center Dr., Lebanon, NH 03756. Phone: (603) 650-7730. Fax: (603) 650-6223. E-mail: edward.j.usherwood{at}dartmouth.edu.

{dagger} Present address: Department of Large Animal Medicine, University of Georgia, Athens.

{ddagger} Present address: Centre for Comparative Infectious Diseases, Department of Medical Microbiology, University of Liverpool, Liverpool, United Kingdom.


Journal of Virology, October 2004, p. 10829-10832, Vol. 78, No. 19
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.19.10829-10832.2004
Copyright © 2004, 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 © 2004 by the American Society for Microbiology. All rights reserved.