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 Schneidewind, A.
Right arrow Articles by Allen, T. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schneidewind, A.
Right arrow Articles by Allen, T. M.

 Previous Article

Journal of Virology, April 2009, p. 3993-3997, Vol. 83, No. 8
0022-538X/09/$08.00+0     doi:10.1128/JVI.01108-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Transmission and Long-Term Stability of Compensated CD8 Escape Mutations{triangledown}

Arne Schneidewind,1,2 Zabrina L. Brumme,1 Chanson J. Brumme,1 Karen A. Power,1 Laura L. Reyor,1 Kristin O'Sullivan,1 Adrianne Gladden,1 Ursula Hempel,1 Thomas Kuntzen,1 Yaoyu E. Wang,1 Cesar Oniangue-Ndza,1 Heiko Jessen,3 Martin Markowitz,4 Eric S. Rosenberg,1 Rafick-Pierre Sékaly,5 Anthony D. Kelleher,6 Bruce D. Walker,1 and Todd M. Allen1*

Partners AIDS Research Center, Massachusetts General Hospital, Boston, Massachusetts,1 Klinik für Innere Medizin I, Universitätsklinikum Regensburg, Regensburg, Germany,2 Jessen-Praxis, Berlin, Germany,3 Aaron Diamond AIDS Research Center, New York, New York,4 Université de Montréal, Montreal, Canada,5 University of New South Wales, Sydney, Australia6

Received 26 May 2008/ Accepted 8 December 2008

Human immunodeficiency virus effectively evades CD8+ T-cell responses through the development of CD8 escape mutations. Recent reports documenting reversion of transmitted mutations and the impact of specific escape mutations upon viral replication suggest that complex forces limit the accumulation of CD8 escape mutations at the population level. However, the presence of compensatory mutations capable of alleviating the impact of CD8 escape mutations on replication capacity may enable their persistence in an HLA-mismatched host. Herein, we illustrate the long-term stability of stereotypic escape mutations in the immunodominant HLA-B27-restricted epitope KK10 in p24/Gag following transmission when accompanied by a specific compensatory mutation.

* Corresponding author. Mailing address: Division of Infectious Diseases, Massachusetts General Hospital, Bldg. 149, 13th St., Rm. 6625, Charlestown, MA 02129. Phone: (617) 726-7846. Fax: (617) 724-8586. E-mail: tallen2{at}partners.org

{triangledown} Published ahead of print on 17 December 2008.

Journal of Virology, April 2009, p. 3993-3997, Vol. 83, No. 8
0022-538X/09/$08.00+0     doi:10.1128/JVI.01108-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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