Failure to complement infectivity of EBV and HSV-1 glycoprotein B (gB) deletion mutants with gBs from different human herpesvirus subfamilies
Failure to complement infectivity of EBV and HSV-1 glycoprotein B (gB) deletion mutants with gBs from different human herpesvirus subfamilies
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DOI：
10.1006/viro.1997.8765
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发表时间：
1997-10-13
期刊：
影响因子：
3.7
通讯作者：
Longnecker, R
中科院分区：
文献类型：
--
作者：
Lee, SK;Compton, T;Longnecker, R
糖蛋白B （gB）在疱疹病毒家族中是保守的，感染范围很广。为了研究人类α -疱疹病毒、β -疱疹病毒和γ -疱疹病毒gB蛋白的功能同源性，利用EBV gp110 （EBV gB同源物）和HSV-1 gB零突变体，对每个亚家族成员的gB基因进行了互补研究。α -疱疹病毒HSV-1 gB基因和β -疱疹病毒HCMV gB基因都不能补充gp110零突变体。相反，β -疱疹病毒HCMV gB或γ -疱疹病毒EBV gp110基因都不能补充HSV-1 gB零突变体。为了进一步研究EBV gp110和HSV-1 gB的功能域，构建了gB-gp110嵌合蛋白。令人惊讶的是，没有一个嵌合蛋白能够补充HSV-1 gB零突变体或EBV gp110零突变体。这些结果表明，不同的gBs之间没有足够的功能同源性，以允许在疱疹病毒家族的其他亚家族成员中互补。(C) 1997学术出版社。
Glycoprotein B (gB) is conserved among the herpesvirus family which infects a broad range of species. To investigate the functional homology of human alpha-herpesviruses, beta-herpesviruses, and gamma-herpesviruses gB proteins, complementation studies were performed with gB genes from each subfamily member using EBV gp110 (EBV gB homologue) and HSV-1 gB null mutants. Neither the alpha-herpesvirus HSV-1 gB gene nor the beta-herpesvirus HCMV gB gene were able to complement the gp110 null mutant. Conversely, neither the beta-herpesvirus HCMV gB or the gamma-herpesvirus EBV gp110 gene were able to complement HSV-1 gB null mutants. To further investigate functional domains of EBV gp110 and HSV-1 gB, gB-gp110 chimeric proteins were constructed. Surprisingly, none of the chimeric proteins were able to complement either HSV-1 gB null mutants or EBV gp110 null mutants. These results demonstrate that there is not sufficient functional homology between the different gBs to allow complementation in other subfamily members of the herpesvirus family. (C) 1997 Academic Press.