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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3360-3366
IMMUNOBIOLOGY
Identification of an HLA A*0201-restricted CD8+
T-cell epitope for the glycoprotein B homolog of human
herpesvirus 8
Qiong J. Wang,
Xiao-Li Huang,
Giovanna Rappocciolo,
Frank J. Jenkins,
William H. Hildebrand,
Zheng Fan,
Elaine K. Thomas, and
Charles R. Rinaldo Jr
From the Department of Infectious Diseases and
Microbiology, Graduate School of Public Health, and the Department of
Pathology, School of Medicine, University of Pittsburgh, Pennsylvania;
the Department of Microbiology and Immunology, University of Oklahoma
Health Sciences Center, Oklahoma City; and the Immunex Corporation,
Seattle, WA.
Human herpesvirus 8 (HHV-8; Kaposi sarcoma-associated
herpesvirus)-specific cytotoxic T-lymphocyte (CTL) and interferon- (IFN-) responses to proteins produced during the lytic cycle of
HHV-8 replication are mediated by HLA class I-restricted,
CD8+ T cells. We have characterized the fine specificity of
the CD8+ T-cell response to 25 peptides derived from 5 HHV-8 lytic cycle proteins based on a prediction model for HLA A*0201
binding motifs. One of the 25 HLA A*0201 peptides derived from the
glycoprotein B (gB) homolog of Epstein-Barr virus
(gB492-500; LMWYELSKI; single-letter amino acid
codes) bound to HLA A*0201 and stimulated IFN- responses in
CD8+ T cells from HHV-8+, HLA A*0201 persons,
but not HHV-8-seronegative or non-HLA A*0201 persons. The peptide
also induced IFN- and CTL reactivity to naturally processed gB
protein. The peptide was a major immunogenic epitope of HHV-8 as
indicated by induction of IFN- responses in peripheral blood
mononuclear cells from 5 of 5 HHV-8 seropositive, HLA A*0201 persons
when gB492-500 was presented by autologous dendritic cells. T-cell reactivity to gB492-500 was not
related to detectable HHV-8 DNA in the blood. These data
show that CD8+ T cells recognize an HLA A*0201-restricted
epitope for HHV-8 lytic cycle protein gB, particularly when presented
by dendritic cells. This epitope may be important in control of HHV-8
infection by CD8+ T cells.
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