Mutch D, Underwood J, Geysen M, Rodda S
Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
J Acquir Immune Defic Syndr (1988). 1994 Sep;7(9):879-90.
Peripheral blood mononuclear cells from 12 asymptomatic human immunodeficiency virus (HIV)-1-seropositive and nine HIV-1-seronegative donors were screened for proliferative T-lymphocyte responses to peptides derived from a consensus sequence of the HIV-1 env gene products from 25 HIV-1 isolates. Two hundred seventy-eight overlapping 17mer peptides, incremented by three residues each, were pooled into groups, each containing eight sequential peptides, for use in proliferation tests. Thirty-eight additional peptides containing variant amino acid residues also were tested. Proliferation data were analyzed using an algorithm that reduced subjective bias and estimated the responding cell frequencies. Peripheral blood mononuclear cells from a majority of donors, regardless of HIV-1 status, recognized peptides within two pools derived from the gp120 sequence and peptides from one pool in gp41. Pool 25 peptides from gp41 (centered around residue 600 of the gp160 consensus sequence) were recognized most frequently. The observed inability to differentiate between responses of HIV-1-seropositive and HIV-1-seronegative individuals implies either a lack of HIV-1 disease-related immunodominant env epitopes or functional abrogation of HIV-1 env-specific T-helper lymphocyte responses soon after infection. The observed proliferation of T lymphocytes from noninfected, low-risk individuals questions the origin of the responses to HIV-1 env-derived peptides and suggest that preexisting, cross-reactive immunity could influence responses to HIV-1.
对12名无症状的人类免疫缺陷病毒(HIV)-1血清阳性供者和9名HIV-1血清阴性供者的外周血单个核细胞进行了筛查,以检测其对来自25株HIV-1分离株的HIV-1 env基因产物共有序列衍生肽的增殖性T淋巴细胞反应。将278个重叠的17肽按每次三个残基递增的方式分组,每组包含八个连续的肽,用于增殖试验。还测试了另外38个含有变异氨基酸残基的肽。使用一种算法分析增殖数据,该算法减少了主观偏差并估计了反应细胞频率。大多数供者的外周血单个核细胞,无论HIV-1状态如何,都能识别来自gp120序列的两个肽池中的肽以及gp41中一个肽池的肽。来自gp41的第25号肽池(以gp160共有序列的第600位残基为中心)被识别的频率最高。观察到无法区分HIV-1血清阳性和HIV-1血清阴性个体的反应,这意味着要么缺乏与HIV-1疾病相关的免疫显性env表位,要么在感染后不久HIV-1 env特异性T辅助淋巴细胞反应发生了功能废除。未感染的低风险个体的T淋巴细胞出现增殖,这对HIV-1 env衍生肽反应的起源提出了质疑,并表明预先存在的交叉反应性免疫可能会影响对HIV-1的反应。