Target Peptide Sequence within Infectious Human Immunodeficiency Virus Type 1 Does Not Ensure Envelope-Specific T-Helper Cell Reactivation: Influences of Cysteine Protease and Gamma Interferon-Induced Thiol Reductase Activities

Author:

Sealy Robert1234,Chaka Wendy1234,Surman Sherri1234,Brown Scott A.1234,Cresswell Peter1234,Hurwitz Julia L.1234

Affiliation:

1. Departments of Infectious Diseases

2. Immunology, St. Jude Children's Research Hospital, 332 N. Lauderdale St., Memphis, Tennessee 38105

3. Department of Immunobiology, Yale University School of Medicine, HHMI, 300 Cedar St., New Haven, Connecticut 06520

4. Department of Pathology, Health Science Center, University of Tennessee, Memphis, Tennessee, 38163

Abstract

ABSTRACT 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.

Publisher

American Society for Microbiology

Subject

Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy

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