Razumov I A, Khusainova A D, Agapov E V, Pereboev A V, Kolykhalov A A, Netesov S V, Loktev V B
Institute of Molecular Biology, State Research Center of Virology and Biotechnology Vector, Koltsovo, Russia.
Intervirology. 1994;37(6):356-60. doi: 10.1159/000150401.
The hemagglutination (HA) domains of the Venezuelan equine encephalomyelitis (VEE) and the eastern equine encephalomyelitis (EEE) viruses providing the interaction of virions and red blood cells were studied with the use of a panel of 17 hemagglutination inhibition (HI) monoclonal antibodies (MAbs). A highly conserved domain (C domain) forming alphavirus-group-reactive MAbs was identified in the E2 protein of the VEE and EEE viruses. These MAbs inhibited HA of the western equine encephalomyelitis, Semliki Forest, Sindbis, Getah, Aura, Chikungunya and Pixuna viruses. The involvement of amino acid residues 59 and 232 in the formation of the C region was demonstrated by sequencing the gene encoding the E2 protein of three escape variants of the VEE virus.
利用一组17种血凝抑制（HI）单克隆抗体（MAb）研究了委内瑞拉马脑炎（VEE）病毒和东部马脑炎（EEE）病毒的血凝（HA）结构域，该结构域介导病毒粒子与红细胞的相互作用。在VEE病毒和EEE病毒的E2蛋白中鉴定出一个形成甲病毒属组反应性MAb的高度保守结构域（C结构域）。这些MAb抑制西部马脑炎病毒、辛德毕斯病毒、Semliki森林病毒、盖塔病毒、奥拉病毒、基孔肯雅病毒和皮苏纳病毒的HA。通过对VEE病毒三个逃逸变异株的E2蛋白编码基因进行测序，证明了氨基酸残基59和232参与C区域的形成。
