Masemola Agatha, Mashishi Tumelo, Khoury Greg, Mohube Phineas, Mokgotho Pauline, Vardas Efthyia, Colvin Mark, Zijenah Lynn, Katzenstein David, Musonda Rosemary, Allen Susan, Kumwenda Newton, Taha Taha, Gray Glenda, McIntyre James, Karim Salim Abdool, Sheppard Haynes W, Gray Clive M
National Institute for Communicable Diseases, Johannesburg, South Africa.
J Virol. 2004 Apr;78(7):3233-43. doi: 10.1128/jvi.78.7.3233-3243.2004.
An understanding of the relationship between the breadth and magnitude of T-cell epitope responses and viral loads is important for the design of effective vaccines. For this study, we screened a cohort of 46 subtype C human immunodeficiency virus type 1 (HIV-1)-infected individuals for T-cell responses against a panel of peptides corresponding to the complete subtype C genome. We used a gamma interferon ELISPOT assay to explore the hypothesis that patterns of T-cell responses across the expressed HIV-1 genome correlate with viral control. The estimated median time from seroconversion to response for the cohort was 13 months, and the order of cumulative T-cell responses against HIV proteins was as follows: Nef > Gag > Pol > Env > Vif > Rev > Vpr > Tat > Vpu. Nef was the most intensely targeted protein, with 97.5% of the epitopes being clustered within 119 amino acids, constituting almost one-third of the responses across the expressed genome. The second most targeted region was p24, comprising 17% of the responses. There was no correlation between viral load and the breadth of responses, but there was a weak positive correlation (r = 0.297; P = 0.034) between viral load and the total magnitude of responses, implying that the magnitude of T-cell recognition did not contribute to viral control. When hierarchical patterns of recognition were correlated with the viral load, preferential targeting of Gag was significantly (r = 0.445; P = 0.0025) associated with viral control. These data suggest that preferential targeting of Gag epitopes, rather than the breadth or magnitude of the response across the genome, may be an important marker of immune efficacy. These data have significance for the design of vaccines and for interpretation of vaccine-induced responses.
了解T细胞表位反应的广度和强度与病毒载量之间的关系对于设计有效的疫苗至关重要。在本研究中,我们对46名感染1型C亚型人类免疫缺陷病毒(HIV-1)的个体组成的队列进行了筛查,以检测其针对一组与完整C亚型基因组对应的肽段的T细胞反应。我们使用γ干扰素酶联免疫斑点分析来探究以下假设:在表达的HIV-1基因组上的T细胞反应模式与病毒控制相关。该队列从血清转化到出现反应的估计中位时间为13个月,针对HIV蛋白的累积T细胞反应顺序如下:Nef>Gag>Pol>Env>Vif>Rev>Vpr>Tat>Vpu。Nef是最常被靶向的蛋白,97.5%的表位聚集在119个氨基酸内,占整个表达基因组反应的近三分之一。第二个最常被靶向的区域是p24,占反应的17%。病毒载量与反应广度之间没有相关性,但病毒载量与反应的总强度之间存在弱正相关(r = 0.297;P = 0.034),这意味着T细胞识别的强度对病毒控制没有贡献。当将识别的分层模式与病毒载量相关联时,对Gag的优先靶向与病毒控制显著相关(r = 0.445;P = 0.0025)。这些数据表明,对Gag表位的优先靶向,而非整个基因组反应的广度或强度,可能是免疫效力的一个重要标志。这些数据对于疫苗设计和疫苗诱导反应的解释具有重要意义。