血凝素残基的附近簇维持了依赖信号淋巴细胞激活分子的犬瘟热病毒在外周血单核细胞中的进入。
Nearby clusters of hemagglutinin residues sustain SLAM-dependent canine distemper virus entry in peripheral blood mononuclear cells.
作者信息
von Messling Veronika, Oezguen Numan, Zheng Qi, Vongpunsawad Sompong, Braun Werner, Cattaneo Roberto
机构信息
Molecular Medicine Program, Mayo Clinic, Guggenheim 1838, 200 1st Street SW, Rochester, MN 55905, USA.
出版信息
J Virol. 2005 May;79(9):5857-62. doi: 10.1128/JVI.79.9.5857-5862.2005.
Abstract
Signaling lymphocytic activation molecule (SLAM, CD150) is the universal morbillivirus receptor. Based on the identification of measles virus (MV) hemagglutinin (H) amino acids supporting human SLAM-dependent cell entry, we mutated canine distemper virus (CDV) H and identified residues necessary for efficient canine SLAM-dependent membrane fusion. These residues are located in two nearby clusters in a new CDV H structural model. To completely abolish SLAM-dependent fusion, combinations of mutations were necessary. We rescued a SLAM-blind recombinant CDV with six mutations that did not infect ferret peripheral blood mononuclear cells while retaining full infectivity in epithelial cells.
摘要
信号淋巴细胞激活分子（SLAM，CD150）是普遍的麻疹病毒受体。基于对支持人源SLAM依赖性细胞进入的麻疹病毒（MV）血凝素（H）氨基酸的鉴定，我们对犬瘟热病毒（CDV）H进行了突变，并确定了高效的犬源SLAM依赖性膜融合所必需的残基。这些残基位于新的CDV H结构模型中两个相邻的簇中。为了完全消除SLAM依赖性融合，需要进行突变组合。我们拯救了一种具有六个突变的SLAM缺陷型重组CDV，该病毒不感染雪貂外周血单核细胞，同时在上皮细胞中保留完全的感染性。
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