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1887

Journal of General Virology header logo Journal of General Virology

Volume 87, Issue 1

Screening for CD8 cytotoxic T lymphocytes specific for Gag of human immunodeficiency virus type 1 subtype B′ Henan isolate from China and identification of novel epitopes restricted by the HLA-A2 and HLA-A11 alleles No Access

Abstract

The human immunodeficiency virus type 1 (HIV-1) epidemic in China is increasing rapidly at an irrepressible rate. It is caused by HIV-1 subtype B′ in central China. After the full-length genome sequencing of the Henan isolate was performed, the definition of optimal cytotoxic T-lymphocyte (CTL) epitopes across the Henan isolate genome has become crucial for vaccine design. In this study, by using ELISPOT assays with synthetic peptides corresponding to the sequence of the Henan isolate, the identification and analysis of Gag-specific CTL responses among 28 treated and 26 untreated infected paid blood donors (PBDs) from the Henan and Hubei provinces of China are presented. These studies focused on CTL responses restricted by the human leukocyte antigen (HLA)-A2 and -A11 molecules, two of the most prominent HLA-A alleles in the Chinese population. The results suggested that, in the subgroup analysis, the magnitude of response in the infected treated subgroup [median, 93 spot-forming cells (SFCs) per 10 peripheral blood mononuclear cells (PBMCs)] was significantly lower than that in the chronically infected untreated subgroup (median, 221 SFCs per 10 PBMCs), and HLA-A2-restricted treated PBDs had a response of a much higher frequency and magnitude than that of HLA-A11-restricted treated PBDs. Moreover, some novel peptides restricted by the HLA-A2 and -A11 molecules were identified.

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2006-01-01
2025-03-19
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/content/journal/jgv/10.1099/vir.0.81335-0
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Screening for CD8 cytotoxic T lymphocytes specific for Gag of human immunodeficiency virus type 1 subtype B′ Henan isolate from China and identification of novel epitopes restricted by the HLA-A2 and HLA-A11 alleles
J. Gen. Virol. 87, 151 (2006); https://doi.org/10.1099/vir.0.81335-0
/content/journal/jgv/10.1099/vir.0.81335-0
/content/journal/jgv/10.1099/vir.0.81335-0
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