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A peptide-loaded dendritic cell based cytotoxic T-lymphocyte (CTL) vaccination strategy using peptides that span SIV Tat, Rev, and Env overlapping reading frames

Zachary Klase1, Michael J Donio1, Andrew Blauvelt345, Preston A Marx6, Kuan-Teh Jeang7 and Stephen M Smith12*

Author Affiliations

1 Department of Infectious Diseases, Saint Michael's Medical Center, Newark, New Jersey, USA

2 Department of Preventive Medicine and Community Health, New Jersey Medical School, Newark, New Jersey, USA

3 Department of Dermatology, Oregon Health & Science University, Portland, Oregon, USA

4 Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, USA

5 Dermatology Service, VA Medical Center, Portland, Oregon, USA

6 Tulane National Primate Research Center, Tulane University Health Sciences Center, Department of Tropical Medicine, Covington, Louisiana, USA

7 Molecular Virology Section, Laboratory of Molecular Medicine, NIAID, NIH, Bethesda, Maryland, USA

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Retrovirology 2006, 3:1  doi:10.1186/1742-4690-3-1

Published: 6 January 2006

Abstract

CTL based vaccine strategies in the macaque model of AIDS have shown promise in slowing the progression to disease. However, rapid CTL escape viruses can emerge rendering such vaccination useless. We hypothesized that such escape is made more difficult if the immunizing CTL epitope falls within a region of the virus that has a high density of overlapping reading frames which encode several viral proteins. To test this hypothesis, we immunized macaques using a peptide-loaded dendritic cell approach employing epitopes in the second coding exon of SIV Tat which spans reading frames for both Env and Rev. We report here that autologous dendritic cells, loaded with SIV peptides from Tat, Rev, and Env, induced a distinct cellular immune response measurable ex vivo. However, conclusive in vivo control of a challenge inoculation of SIVmac239 was not observed suggesting that CTL epitopes within densely overlapping reading frames are also subject to escape mutations.