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Clinical and Vaccine Immunology, April 2008, p. 713-719, Vol. 15, No. 4
1071-412X/08/$08.00+0 doi:10.1128/CVI.00412-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Departments of Infectious Diseases,1 Immunology, St. Jude Children's Research Hospital, 332 N. Lauderdale St., Memphis, Tennessee 38105,2 Department of Immunobiology, Yale University School of Medicine, HHMI, 300 Cedar St., New Haven, Connecticut 06520,3 Department of Pathology, Health Science Center, University of Tennessee, Memphis, Tennessee, 381634
Received 11 October 2007/ Returned for modification 20 November 2007/ Accepted 21 January 2008
Recent clinical trials have shown that the presence of a robust human immunodeficiency virus type 1 (HIV-1)-specific T-cell response may not be sufficient to prevent or control HIV-1 infection. Studies of antigen processing in the context of infectious HIV-1 are therefore warranted. Envelope-specific, major histocompatibility complex class II-restricted murine T-cell hybridomas were tested for responsiveness to splenic antigen-presenting cells exposed to HIV-1-infected GHOST cells. Interleukin-2 assays showed that the presence of a peptide within HIV-1 did not ensure the reactivation of peptide-specific T cells. Further experiments defined the impact of gamma interferon-induced thiol reductase and cysteine proteases on the processing of HIV-1 peptides. The results highlight potential influences of peptide context on T-cell reactivation by HIV-1 and encourage the continued study of antigen processing as support for improved vaccine design.
Published ahead of print on 30 January 2008.
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