Turner Peter C, Moyer Richard W
Department of Molecular Genetics and Microbiology, College of Medicine, University of Florida, Gainesville, FL 32610, USA.
Virology. 2008 Oct 25;380(2):226-33. doi: 10.1016/j.virol.2008.07.020. Epub 2008 Aug 28.
The orthopoxvirus SPI-3 (K2) and A56 (hemagglutinin, HA) proteins interact and together prevent cell-cell fusion. SPI-3/A56 has been proposed to prevent the superinfection of previously infected cells by reducing virus-cell fusion. Binding of mature virions of vaccinia virus (VV) to VV-infected cells was unaffected by SPI-3 or A56 on the surface of infected cells. Entry of VV into infected cells was assessed using VV-P(T7)-luc carrying the luciferase reporter under T7 control. Cells infected with VV or cowpox virus (CPV) expressing T7 RNA polymerase and lacking SPI-3 and/or A56 were superinfected with VV-P(T7)-luc, and luciferase activity was measured. Inactivation of SPI-3 or A56 from the pre-infecting virus resulted in greater luciferase expression from the superinfecting VV-P(T7)-luc. Antibody against SPI-3 present during infection with wild-type CPV-T7 increased luciferase expression from superinfecting VV-P(T7)-luc. The SPI-3/A56 complex on the infected cell surface therefore appears to reduce the entry of virions into infected cells.
正痘病毒SPI-3（K2）蛋白和A56（血凝素，HA）蛋白相互作用，共同防止细胞间融合。有人提出SPI-3/A56通过减少病毒-细胞融合来防止先前感染的细胞发生重复感染。痘苗病毒（VV）成熟病毒粒子与VV感染细胞的结合不受感染细胞表面SPI-3或A56的影响。使用携带T7控制下荧光素酶报告基因的VV-P(T7)-luc评估VV进入感染细胞的情况。用表达T7 RNA聚合酶且缺乏SPI-3和/或A56的VV或牛痘病毒（CPV）感染细胞，然后用VV-P(T7)-luc进行重复感染，并测量荧光素酶活性。从预感染病毒中去除SPI-3或A56会导致重复感染的VV-P(T7)-luc产生更高的荧光素酶表达。在野生型CPV-T7感染期间存在的抗SPI-3抗体增加了重复感染的VV-P(T7)-luc的荧光素酶表达。因此，感染细胞表面的SPI-3/A56复合物似乎减少了病毒粒子进入感染细胞的过程。
