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水泡性口炎病毒糖蛋白中两个保守酸性氨基酸的突变影响pH依赖性构象变化,并降低膜融合的pH阈值。

Mutations at two conserved acidic amino acids in the glycoprotein of vesicular stomatitis virus affect pH-dependent conformational changes and reduce the pH threshold for membrane fusion.

作者信息

Fredericksen B L, Whitt M A

机构信息

Department of Microbiology and Immunology, University of Tennessee at Memphis, 38163, USA.

出版信息

Virology. 1996 Mar 1;217(1):49-57. doi: 10.1006/viro.1996.0092.

DOI:10.1006/viro.1996.0092
PMID:8599235
Abstract

Recently, we had shown that amino acid substitutions at residues 124, 127, and 133 either abolished or drastically altered the fusion activity of the glycoprotein (G protein) of vesicular stomatitis virus (VSV), indicating that this region is important for membrane fusion and may constitute an internal fusion domain. In this report we show that amino acid substitutions at two conserved acidic residues located at the C-terminal end of the putative fusion domain also affect the fusion activity of G protein. Two substitutions, D127-L and E139-L, slightly reduced the pH threshold at which G protein mediates membrane fusion. However, both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below. To determine if the fusion activity of G protein required an acidic residue in this region both D137 and E139 were replaced with serine. This double substitution also reduced the pH threshold for fusion activity, but the effect appeared to be less severe than that for either of the single substitutions. The mutated G protein cDNAs were also introduced into a VSV minigenome to examine the effect of the substitutions on virus assembly and infectivity. All three mutant G proteins assembled into particles and these virions were infectious despite the altered fusion activities of the mutant G proteins. Although particles containing the mutant proteins were infectious they appeared to be attenuated, suggesting that these two acidic residues, which are conserved in several distantly related rhabdoviruses, play an important role in maintaining virus fitness.

摘要

最近,我们已经表明,在水泡性口炎病毒(VSV)糖蛋白(G蛋白)的第124、127和133位残基处的氨基酸替换,要么消除要么显著改变了该糖蛋白的融合活性,这表明该区域对于膜融合很重要,可能构成一个内部融合结构域。在本报告中,我们表明,在假定融合结构域C末端的两个保守酸性残基处的氨基酸替换也会影响G蛋白的融合活性。两个替换,D127-L和E139-L,略微降低了G蛋白介导膜融合的pH阈值。然而,在暴露于pH 5.7或更低的pH值后,D137-L和E139-L的融合活性都与野生型G蛋白相当。为了确定G蛋白的融合活性是否需要该区域中的酸性残基,将D137和E139都替换为丝氨酸。这种双重替换也降低了融合活性的pH阈值,但效果似乎比任何一个单一替换都要轻。突变的G蛋白cDNA也被引入到VSV微型基因组中,以检查这些替换对病毒组装和感染性的影响。尽管突变G蛋白的融合活性发生了改变,但所有三种突变G蛋白都组装成了颗粒,并且这些病毒粒子具有感染性。虽然含有突变蛋白的颗粒具有感染性,但它们似乎被减弱了,这表明在几种远缘相关的弹状病毒中保守的这两个酸性残基在维持病毒适应性方面起着重要作用。

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