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Genetic Analysis of the Herpes Simplex Virus Type 1 UL20 Protein Domains Involved in Cytoplasmic Virion Envelopment and Virus-Induced Cell Fusion

机译:单纯性疱疹病毒1型UL20蛋白域参与细胞质病毒膜包膜和病毒诱导的细胞融合的遗传分析。

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摘要

The herpes simplex virus type 1 UL20 protein (UL20p) is an important determinant for cytoplasmic virion morphogenesis and virus-induced cell fusion. To delineate the functional domains of the UL20 protein, we generated a panel of single and multiple (cluster) alanine substitutions as well as UL20p carboxyl-terminal truncations. The UL20 mutant genes could be broadly categorized into four main groups: Group I UL20 mutant genes complemented for both virus production and virus-induced cell fusion; Group II UL20 mutant genes did not complement for either virus-induced cell fusion or infectious virus production; Group III UL20 mutant genes complemented for virus-induced cell fusion to variable extents but exhibited substantially decreased ability to complement UL20-null infectious virus production; Group IV mutant genes complemented for infectious virus production but had variable effects on virus-induced cell fusion; this group included two mutants that efficiently complemented for gBsyn3, but not for gKsyn1, virus-induced cell fusion. In addition, certain recombinant viruses with mutations in either the amino or carboxyl termini of UL20p produced partially syncytial plaques on Vero cells in the absence of any other virally encoded syncytial mutations. These studies indicated that the amino and carboxyl termini of UL20p contained domains that functioned both in infectious virus production and virus-induced cell fusion. Moreover, the data suggested that the UL20p's role in virus-induced cell fusion can be functionally separated from its role in cytoplasmic virion morphogenesis and that certain UL20p domains that function in gB-syn3 virus-induced cell fusion are distinct from those functioning in gKsyn1 virus-induced cell fusion.
机译:单纯疱疹病毒1型UL20蛋白(UL20p)是细胞质病毒体形态发生和病毒诱导的细胞融合的重要决定因素。为了描述UL20蛋白的功能域,我们生成了一组单个和多个(簇)丙氨酸取代以及UL20p羧基末端截短。 UL20突变基因可大致分为四个主要类别:I类UL20突变基因,可同时用于病毒生产和病毒诱导的细胞融合; II组UL20突变基因不能补充病毒诱导的细胞融合或感染性病毒的产生。 III组UL20突变基因可在不同程度上补充病毒诱导的细胞融合,但对UL20无感染性病毒产生的补充能力却大大降低。 IV组突变基因可补充感染性病毒的产生,但对病毒诱导的细胞融合具有可变的影响。该组包括两个突变体,它们有效地补充了gBsyn3,但不补充gKsyn1,即病毒诱导的细胞融合。此外,在没有任何其他病毒编码合胞体突变的情况下,某些在UL20p的氨基或羧基末端具有突变的重组病毒在Vero细胞上产生了部分合胞体斑块。这些研究表明,UL20p的氨基和羧基末端包含在感染性病毒生产和病毒诱导的细胞融合中均起作用的结构域。此外,数据表明UL20p在病毒诱导的细胞融合中的作用可以从功能上与它在细胞质病毒体形态发生中的作用分开,并且某些在gB-syn3病毒诱导的细胞融合中起作用的UL20p域与在gKsyn1病毒中起作用的域不同诱导的细胞融合。

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