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Journal of Virology, April 2005, p. 4580-4588, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4580-4588.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Vaccine-Elicited Memory Cytotoxic T Lymphocytes Contribute to Mamu-A*01-Associated Control of Simian/Human Immunodeficiency Virus 89.6P Replication in Rhesus Monkeys

Michael S. Seaman,1 Sampa Santra,1 Michael H. Newberg,1 Valerie Philippon,2 Kelledy Manson,2 Ling Xu,3 Rebecca S. Gelman,4 Dennis Panicali,2 John R. Mascola,3 Gary J. Nabel,3 and Norman L. Letvin1,3*

Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School,1 Department of Biostatistics, Dana-Farber Cancer Institute, Boston,4 Therion Biologics, Cambridge, Massachusetts,2 Vaccine Research Center, National Institutes of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland3

Received 18 October 2004/ Accepted 6 December 2004

The expression of particular major histocompatibility complex (MHC) class I alleles can influence the rate of disease progression following lentiviral infections. This effect is a presumed consequence of potent cytotoxic T-lymphocyte (CTL) responses that are restricted by these MHC class I molecules. The present studies have examined the impact of the MHC class I allele Mamu-A*01 on simian/human immunodeficiency virus 89.6P (SHIV-89.6P) infection in unvaccinated and vaccinated rhesus monkeys by exploring the contribution of dominant-epitope specific CTL in this setting. Expression of Mamu-A*01 in immunologically naive monkeys was not associated with improved control of viral replication, CD4+ T-lymphocyte loss, or survival. In contrast, Mamu-A*01+ monkeys that had received heterologous prime/boost immunizations prior to challenge maintained higher CD4+ T-lymphocyte levels and better control of SHIV-89.6P replication than Mamu-A*01– monkeys. This protection was associated with the evolution of high-frequency anamnestic CTL responses specific for a dominant Mamu-A*01-restricted Gag epitope following infection. These data indicate that specific MHC class I alleles can confer protection in the setting of a pathogenic SHIV infection by their ability to elicit memory CTL following vaccination.

* Corresponding author. Mailing address: Beth Israel Deaconess Medical Center, Division of Viral Pathogenesis, 330 Brookline Ave. RE-113, Boston, MA 02215. Phone: (617) 667-2766. Fax: (617) 667-8210. E-mail: nletvin{at}bidmc.harvard.edu.

Journal of Virology, April 2005, p. 4580-4588, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4580-4588.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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