Brum Lauren M, Turner Peter C, Devick Heather, Baquero M Teresa, Moyer Richard W
Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL 32610, USA.
Virology. 2003 Feb 15;306(2):289-302. doi: 10.1016/s0042-6822(02)00017-x.
The cowpox virus (CPV) glycoprotein serpin SPI-3, a functional protease inhibitor, and the viral hemagglutinin (HA) are required to prevent fusion of wt CPV infected cells. SPI-3 and HA from CPV infected cells co-localize to the plasma membrane and are found in extracellular enveloped virus (EEV). We also show that an N-terminal SPI-3 signal sequence, but not glycosylation, is required for membrane localization and fusion inhibition. In the absence of HA (CPVDeltaHA), no SPI-3 is found on the membrane and infected cells fuse. Conversely, HA from both wt CPV and CPVDeltaSPI-3 infections is on the membrane, indicating a requirement of HA for SPI-3 plasma membrane localization. In the absence of HA, secretion of SPI-3 or SPI-3 N-glyc(-) was markedly enhanced, suggesting HA serves to retain SPI-3 on the plasma membrane,thereby preventing cell fusion.
牛痘病毒（CPV）糖蛋白丝氨酸蛋白酶抑制剂SPI-3是一种功能性蛋白酶抑制剂，病毒血凝素（HA）对于防止野生型CPV感染细胞融合是必需的。来自CPV感染细胞的SPI-3和HA共定位于质膜，并存在于细胞外被膜病毒（EEV）中。我们还表明，膜定位和融合抑制需要SPI-3的N端信号序列，而不是糖基化。在没有HA（CPVDeltaHA）的情况下，在膜上未发现SPI-3，感染的细胞发生融合。相反，野生型CPV和CPVDeltaSPI-3感染产生的HA都存在于膜上，表明HA是SPI-3质膜定位所必需的。在没有HA的情况下，SPI-3或SPI-3 N-糖基化缺失（SPI-3 N-glyc(-)）的分泌明显增强，这表明HA有助于将SPI-3保留在质膜上，从而防止细胞融合。
