Human Immunodeficiency Virus-Specific Gamma Interferon Enzyme-Linked Immunospot Assay Responses Targeting Specific Regions of the Proteome during Primary Subtype C Infection Are Poor Predictors of the Course of Viremia and Set Point
Human Immunodeficiency Virus-Specific Gamma Interferon Enzyme-Linked Immunospot Assay Responses Targeting Specific Regions of the Proteome during Primary Subtype C Infection Are Poor Predictors of the Course of Viremia and Set Point
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DOI：
10.1128/jvi.01678-08
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发表时间：
2009-01-01
影响因子：
5.4
通讯作者：
Karim, Salim Abdool
中科院分区：
文献类型：
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作者：
Gray, Clive M.;Mlotshwa, Mandla;Karim, Salim Abdool
目前尚不清楚急性感染期间人类免疫缺陷病毒（HIV）特异性T细胞反应的模式是否会影响病毒的设定点和病程。我们希望确定感染后3个月时HIV-1特异性T细胞应答的幅度和宽度是否与12个月时的病毒载量设定点相关，并假设初次感染期间HIV特异性T细胞应答的幅度和宽度将预测设定点。γ干扰素（IFN-γ）酶联免疫斑点（ELISPOT）测定反应在整个蛋白质组中测量47个亚型C HIV-1感染的参与者在感染后12周的中位数。当校正氨基酸长度和个体对每个区域的响应时，识别顺序如下：Nef > Gag > Pol > Rev > Vpr > Env > Vpu > Vif >达特。Nef应答显著（P < 0.05）显性，靶向6个表位区域，与病毒血症病程无关。虽然在快速进展者中存在宽度增加的趋势（平均4 - 7个池），但每个蛋白质区域的反应幅度和宽度与疾病进展无显著差异。IFN-γ应答的幅度和宽度与12个月时的病毒设定点的相关性显示每个蛋白质区域几乎为零。总之，这些数据表明，IFN-γ ELISPOT检测反应的幅度和广度在感染后3个月是无关的疾病的过程中的第一年的感染，并没有相关的，并有低预测能力，在12个月的病毒设定点。
It is unknown whether patterns of human immunodeficiency virus (HIV)-specific T-cell responses during acute infection may influence the viral set point and the course of disease. We wished to establish whether the magnitude and breadth of HIV type 1 (HIV-1)-specific T-cell responses at 3 months postinfection were correlated with the viral-load set point at 12 months and hypothesized that the magnitude and breadth of HIV-specific T-cell responses during primary infection would predict the set point. Gamma interferon (IFN-gamma) enzyme-linked immunospot (ELISPOT) assay responses across the complete proteome were measured in 47 subtype C HIV-1-infected participants at a median of 12 weeks postinfection. When corrected for amino acid length and individuals responding to each region, the order of recognition was as follows: Nef > Gag > Pol > Rev > Vpr > Env > Vpu > Vif > Tat. Nef responses were significantly (P < 0.05) dominant, targeted six epitopic regions, and were unrelated to the course of viremia. There was no significant difference in the magnitude and breadth of responses for each protein region with disease progression, although there was a trend of increased breadth (mean, four to seven pools) in rapid progressors. Correlation of the magnitude and breadth of IFN-gamma responses with the viral set point at 12 months revealed almost zero association for each protein region. Taken together, these data demonstrate that the magnitude and breadth of IFN-gamma ELISPOT assay responses at 3 months postinfection are unrelated to the course of disease in the first year of infection and are not associated with, and have low predictive power for, the viral set point at 12 months.