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Unexpected Diversity of Cellular Immune Responses against Nef and Vif in HIV-1-Infected Patients Who Spontaneously Control Viral Replication
Authors:Leandro F Tarosso  Mariana M Sauer  Sabri Sanabani  Maria Teresa Giret  Helena I Tomiyama  John Sidney  Shari M Piaskowski  Ricardo S Diaz  Ester C Sabino  Alessandro Sette  Jorge Kalil-Filho  David I Watkins  Esper G Kallas
Institution:1. Clinical Immunology and Allergy Division, University of Sao Paulo, Sao Paulo, Brazil.; 2. Division of Infectious Diseases, Federal University of Sao Paulo, Sao Paulo, Brazil.; 3. Sao Paulo Blood Bank, Sao Paulo, Brazil.; 4. La Jolla Institute for Allergy and Immunology, La Jolla, California, United States of America.; 5. Department of Pathology, Medical School, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.;University of Toronto, Canada
Abstract:

Background

HIV-1-infected individuals who spontaneously control viral replication represent an example of successful containment of the AIDS virus. Understanding the anti-viral immune responses in these individuals may help in vaccine design. However, immune responses against HIV-1 are normally analyzed using HIV-1 consensus B 15-mers that overlap by 11 amino acids. Unfortunately, this method may underestimate the real breadth of the cellular immune responses against the autologous sequence of the infecting virus.

Methodology and Principal Findings

Here we compared cellular immune responses against nef and vif-encoded consensus B 15-mer peptides to responses against HLA class I-predicted minimal optimal epitopes from consensus B and autologous sequences in six patients who have controlled HIV-1 replication. Interestingly, our analysis revealed that three of our patients had broader cellular immune responses against HLA class I-predicted minimal optimal epitopes from either autologous viruses or from the HIV-1 consensus B sequence, when compared to responses against the 15-mer HIV-1 type B consensus peptides.

Conclusion and Significance

This suggests that the cellular immune responses against HIV-1 in controller patients may be broader than we had previously anticipated.
Keywords:
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