Communication between S1N330 and a region in S2 of murine coronavirus spike protein is important for virus entry into cells expressing CEACAM1b receptor.
Communication between S1N330 and a region in S2 of murine coronavirus spike protein is important for virus entry into cells expressing CEACAM1b receptor.
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DOI：
10.1006/viro.2002.1391
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发表时间：
2002-03-30
期刊：
影响因子：
3.7
通讯作者：
Taguchi F
中科院分区：
文献类型：
--
作者：
Matsuyama S;Taguchi F
从鼠冠状病毒小鼠肝炎病毒（MHV）JHMV分离的可溶性受体抗性（srr）突变体srr 7和srr 11分别在刺突（S）蛋白的1114位（Leu至Phe）和65位（Leu至His）具有氨基酸突变。这些突变体不能有效感染表达CEACAM 1b（BHK-R2）的BHK细胞，因为它们进入该细胞系的能力低，尽管它们以与野生型（wt）JHMV cl-2相似的方式感染表达CEACAM 1a（BHK-R1）的细胞（松山和田口，病毒学273，80-89，2000）。在这些突变体通过BHK-R2细胞反复传代后，不再从srr 11感染的细胞中分离出病毒，而从srr 7感染的细胞中获得了两种不同的突变体srr 7A和srr 7 B。srr 7A和srr 7 B比srr 7生长高2log 10，并在BHK-R2细胞中诱导融合，与野生型病毒相似。除了源于亲本srr 7的1114位氨基酸变化外，srr 7A和srr 7 B在280位附近有突变，对应于迄今为止检查的所有MHV毒株共有的S1 N330受体结合位点（S1 N330-III）的第三个区域。Srr 7A和srr 7 B S蛋白在BHK-R1和BHK-R2细胞中都显示出高融合性，与野生型病毒一样，而在S1 N330-III中具有突变但在氨基酸1114处没有突变的srr 7Aa和srr 7 Ba S蛋白在这些细胞系中表现出显著降低的融合活性。这些发现表明，S1 N330-III和1114位氨基酸之间的通讯对于BHK-R2细胞中的有效融合活性是重要的。S1 N330-III是S1中参与病毒进入细胞的可能区域。
The soluble receptor-resistant (srr) mutants, srr7 and srr11, isolated from a murine coronavirus, mouse hepatitis virus (MHV) JHMV, have an amino acid mutation at positions 1114 (Leu to Phe) and 65 (Leu to His), respectively, in the spike (S) protein. These mutants failed to efficiently infect BHK cells expressing CEACAM1b (BHK-R2), due to their low entry into this cell line, although they infected cells expressing CEACAM1a (BHK-R1) in a manner similar to that of wild-type (wt) JHMV cl-2 (Matsuyama and Taguchi, Virology 273, 80–89, 2000). Following the repeated passage of these mutants through BHK-R2 cells, viruses were no longer isolated from srr11-infected cells, while two distinct mutants, srr7A and srr7B, were obtained from srr7-infected cells. Srr7A and srr7B grew 2 log10 higher than srr7 and induced fusion in BHK-R2 cells, being similar to wt virus. In addition to the amino acid change at position 1114 that stemmed from parental srr7, srr7A and srr7B had mutations around position 280, corresponding to the third region of the S1N330 receptor-binding site (S1N330-III) common to all MHV strains examined thus far. Srr7A and srr7B S proteins showed high fusogenicity in both BHK-R1 and BHK-R2 cells, like the wt virus, while srr7Aa and srr7Ba S proteins, which had mutations in S1N330-III but not at amino acid 1114, exhibited profoundly reduced fusion activity in these cell lines. These findings suggest that communication between S1N330-III and the amino acid at position 1114 is important for efficient fusion activity in BHK-R2 cells. S1N330-III is a possible region in the S1 involved in viral entry into cells.
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