Blomberg J, Lawoko A, Pipkorn R, Moyo S, Malmvall B E, Shao J, Dash R, Tswana S
Department of Medical Microbiology, University of Lund, Sweden.
AIDS. 1993 Jun;7(6):759-67. doi: 10.1097/00002030-199306000-00002.
To determine whether the known sequence differences between African and non-African HIV-1 strains are reflected in the serological response.
We investigated the antibody reactivity of 34 Swedish, 30 Tanzanian and 42 Zimbabwean HIV-1-positive sera to 67 synthetic peptides with sequences from North American and African HIV-1 isolates, mostly derived from regions of gag and env known to be antigenic. Not all sera were tested against all peptides.
Differences in frequency of reactivity were noted with peptides covering the entire third variable domain (V3), which is a primary neutralization determinant, and the carboxyl terminus of gp120, in two regions of gp41, and the carboxyl terminus of p24. In env Tanzanian sera reacted preferentially with a V3 peptide from the strain JY1 (Zaire). Gradual substitutions in the central motif in V3 of ELI from GLGQ to GPGR, typical of many non-African strains, led to a gradual increase in reactivity of many Swedish sera, but did not affect Tanzanian and Zimbabwean sera, suggesting that the major epitopes recognized by these African sera are outside GPGR. V3 peptides from the MN and Z3 strains reacted with most sera, but missed 30% of those of Tanzanian origin. In the carboxyl terminus of gp120 both sets of African sera reacted preferentially with peptides from strains JY1 and MAL. Swedish sera reacted strongest with analogues from strains Z321 and HXB2. In gp41, Swedish sera showed a weak preference for reactivity with HXB2-derived peptides in the immunodominant region (amino acids 590-620), and further towards the carboxyl terminus (amino acids 620-665).
The differences in serological reactivity were as great between Zimbabwe and Tanzania as between the two African sets and the Swedish. The geographical differences in the pattern of reactivity with HIV peptides probably depend on both host and viral variation and may be developed into a seroepidemiological tool, useful for optimization of future HIV vaccines.
确定非洲和非非洲HIV-1毒株之间已知的序列差异是否反映在血清学反应中。
我们研究了34份瑞典、30份坦桑尼亚和42份津巴布韦HIV-1阳性血清对67种合成肽的抗体反应性，这些合成肽的序列来自北美和非洲的HIV-1分离株，大部分来自已知具有抗原性的gag和env区域。并非所有血清都针对所有肽进行了检测。
在覆盖整个第三可变区（V3）（这是一个主要的中和决定簇）、gp120的羧基末端、gp41的两个区域以及p24的羧基末端的肽中，观察到反应频率的差异。在env中，坦桑尼亚血清优先与来自JY1株（扎伊尔）的V3肽发生反应。ELI的V3中央基序中从GLGQ到GPGR的逐渐取代是许多非非洲毒株的典型特征，这导致许多瑞典血清的反应性逐渐增加，但不影响坦桑尼亚和津巴布韦血清，这表明这些非洲血清识别的主要表位在GPGR之外。来自MN和Z3株的V3肽与大多数血清发生反应，但遗漏了30%的坦桑尼亚来源血清。在gp120的羧基末端，两组非洲血清都优先与来自JYl和MAL株的肽发生反应。瑞典血清与来自Z321和HXB2株的类似物反应最强。在gp41中，瑞典血清在免疫优势区域（氨基酸590 - 620）以及更靠近羧基末端（氨基酸620 - 665）对来自HXB2的肽的反应性表现出微弱的偏好。
津巴布韦和坦桑尼亚之间的血清学反应差异与两组非洲血清和瑞典血清之间的差异一样大。与HIV肽反应模式的地理差异可能取决于宿主和病毒的变异，并且可能发展成为一种血清流行病学工具，有助于优化未来的HIV疫苗。
