6K基因缺失的辛德毕斯病毒变体在糖蛋白加工和运输方面存在缺陷：野生型6K基因反式互补无效。
Sindbis virus variant with a deletion in the 6K gene shows defects in glycoprotein processing and trafficking: lack of complementation by a wild-type 6K gene in trans.
作者信息
Sanz M A, Carrasco L
机构信息
Centro de Biología Molecular, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain.
出版信息
J Virol. 2001 Aug;75(16):7778-84. doi: 10.1128/JVI.75.16.7778-7784.2001.
Abstract
A Sindbis virus (SV) variant with a 6K gene partially deleted has been obtained. This SV Del6K virus is defective in the proteolytic processing of virus glycoprotein precursor, transport of glycoproteins to the plasma membrane, and plaque phenotype. A revertant virus (SV Del6K-revQ21L) containing a point mutation in the deleted 6K gene was isolated and characterized. SV Del6K-revQ21L has corrected the defects of proteolytic processing and transport of virus glycoproteins to the plasma membrane, but it still remains attenuated compared to wild-type (wt) SV, exhibiting defects in virus budding. Neither mutant nor revertant viruses are complemented by the coexpression in trans of a wt SV 6K gene.
摘要
已获得一种6K基因部分缺失的辛德毕斯病毒（SV）变体。这种SV Del6K病毒在病毒糖蛋白前体的蛋白水解加工、糖蛋白向质膜的转运以及蚀斑表型方面存在缺陷。分离并鉴定了一种在缺失的6K基因中含有一个点突变的回复病毒（SV Del6K-revQ21L）。SV Del6K-revQ21L已纠正了病毒糖蛋白的蛋白水解加工和向质膜转运的缺陷，但与野生型（wt）SV相比仍表现出减毒，在病毒出芽方面存在缺陷。野生型SV 6K基因的反式共表达均不能互补突变病毒和回复病毒。
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