Measles virus-substance P receptor interactions. Possible novel mechanism of viral fusion.
Measles virus-substance P receptor interactions. Possible novel mechanism of viral fusion.
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麻疹病毒-P 物质受体相互作用。
DOI：
10.1172/jci114571
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Payan,DG
中科院分区：
文献类型：
--
作者：
Harrowe,G;Mitsuhashi,M;Payan,DG
麻疹病毒（MV）编码的融合蛋白（F）介导病毒的细胞融合和细胞间传播，并且与神经肽物质P（SP）的羧基端同源。此外，与F和SP同源的寡肽Z-D-Phe-L-Phe-Gly也抑制MV与靶细胞的融合。这些观察结果提出了MV是否在其感染周期的特定阶段使用SP受体（SPR）的问题。在这份报告中，我们研究了这种相互作用的结构和功能的后果，并显示，使用交联研究，MV和SP特异性结合到一个52-58 kD的蛋白质，以前报道，包括对人类IM-9成淋巴细胞的SPR。此外，结合的MV和SP显示从这些细胞中相互置换。此外，我们证明，抗SP抗血清抑制MV的细胞间传播，SP阻断MV与靶细胞的融合。这些结果表明在病毒融合过程中存在MV-SPR相互作用，并提出了病毒进入细胞的可能新机制。图片
Measles virus (MV) encodes the fusion protein (F) that mediates cell fusion and intercellular spread of the virus, and is homologous to the carboxy terminus of the neuropeptide substance P (SP). In addition, the oligopeptide Z-D-Phe-L-Phe-Gly, also homologous to F and SP, inhibits MV fusion with target cells. These observations raise the question of whether MV uses the SP receptor (SPR) during a specific phase of its infectious cycle. In this report, we examine the structural and functional consequences of this interaction and show, using cross-linking studies, that MV and SP specifically bind to a 52-58-kD protein, previously reported to comprise the SPR on human IM-9 lymphoblasts. Moreover, bound MV and SP are shown to reciprocally displace each other from these cells. In addition, we demonstrate that anti-SP antisera inhibits the cell-to-cell spread of MV, and that SP blocks MV fusion with target cells. These results indicate the presence of MV-SPR interactions during viral fusion, and suggest possible novel mechanisms for viral entry into cells.Images