牛免疫缺陷病毒包膜核心的特征：对牛免疫缺陷病毒介导的细胞融合机制的启示

Characterization of BIV Env core: implication for mechanism of BIV-mediated cell fusion.

作者信息

Li Shu, Zhu Jieqing, Peng Yu, Cui Shanshan, Wang Chunping, Gao George F, Tien Po

机构信息

Modern Virology Research Center, State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.

出版信息

Biochem Biophys Res Commun. 2005 Apr 8;329(2):603-9. doi: 10.1016/j.bbrc.2005.01.160.

DOI:10.1016/j.bbrc.2005.01.160

PMID:15737628

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7117376/

Abstract

Entry of lentiviruses, such as human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV), requires folding of two heptad repeat regions (HR1 and HR2) of gp41 into a trimer-of-hairpins, which subsequently brings virus and cell membrane into fusion. This motif is a generalized feature of viral fusion proteins and has been exploited in generating antiviral fusion agents. In the present paper, we report structural characters of Env protein from another lentivirus, bovine immunodeficiency virus (BIV), which contributes to a good animal model of HIV. BIV HR1 and HR2 regions are predicted by two different programs and expressed separately or conjointly in Escherichia coli. Biochemical and biophysical analyses show that the predicted HRs of BIV Env can form a stable trimer-of-hairpins or six-helix bundle just like that formed by feline immunodeficiency virus Env. Cell fusion assay demonstrates that the HR2 peptide of BIV can efficiently inhibit the virus-mediated cell fusion.

摘要

慢病毒（如1型人类免疫缺陷病毒（HIV-1）和猴免疫缺陷病毒（SIV））的进入需要将糖蛋白41（gp41）的两个七肽重复区域（HR1和HR2）折叠成发夹三聚体，随后使病毒与细胞膜融合。这种基序是病毒融合蛋白的普遍特征，并已被用于开发抗病毒融合剂。在本文中，我们报告了另一种慢病毒——牛免疫缺陷病毒（BIV）的Env蛋白的结构特征，该病毒有助于建立良好的HIV动物模型。通过两种不同的程序预测BIV的HR1和HR2区域，并在大肠杆菌中分别或联合表达。生化和生物物理分析表明，BIV Env预测的HRs可以形成稳定的发夹三聚体或六螺旋束，就像猫免疫缺陷病毒Env形成的那样。细胞融合试验表明，BIV的HR2肽可以有效抑制病毒介导的细胞融合。