Open AccessIdentification of Novel HLA-A2-Restricted Human Immunodeficiency Virus Type 1-Specific Cytotoxic T-Lymphocyte Epitopes Predicted by the HLA-A2 Supertype Peptide-Binding Motif
Author(s) -
Marcus Altfeld,
Brian Livingston,
Neha Reshamwala,
Phuong Nguyen,
Marylyn M. Addo,
Amy Shea,
Mark J. Newman,
John Fikes,
John Sidney,
Peggy Wentworth,
Robert W. Chesnut,
Robert L. Eldridge,
Eric Rosenberg,
Gregory K. Robbins,
Christian Berthou,
Paul E. Sax,
Steve Boswell,
Theresa Flynn,
Susan Buchbinder,
Philip Goulder,
Bruce D. Walker,
Alessandro Sette,
Spyros A. Kalams
Publication year - 2001
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.75.3.1301-1311.2001
Subject(s) - ctl* , epitope , biology , virology , immunogenicity , cytotoxic t cell , human leukocyte antigen , immunology , major histocompatibility complex , virus , antigen , cd8 , genetics , in vitro
Virus-specific cytotoxic T-lymphocyte (CTL) responses are critical in the control of human immunodeficiency virus type 1 (HIV-1) infection and will play an important part in therapeutic and prophylactic HIV-1 vaccines. The identification of virus-specific epitopes that are efficiently recognized by CTL is the first step in the development of future vaccines. Here we describe the immunological characterization of a number of novel HIV-1-specific, HLA-A2-restricted CTL epitopes that share a high degree of conservation within HIV-1 and a strong binding to different alleles of the HLA-A2 superfamily. These novel epitopes include the first reported CTL epitope in the Vpr protein. Two of the novel epitopes were immunodominant among the HLA-A2-restricted CTL responses of individuals with acute and chronic HIV-1 infection. The novel CTL epitopes identified here should be included in future vaccines designed to induce HIV-1-specific CTL responses restricted by the HLA-A2 superfamily and will be important to assess in immunogenicity studies in infected persons and in uninfected recipients of candidate HIV-1 vaccines.