Yamada Y K, Takimoto K, Yabe M, Taguchi F
National Institute of Infectious Diseases, Tokyo, Japan.
Adv Exp Med Biol. 1998;440:89-93. doi: 10.1007/978-1-4615-5331-1_12.
The spike (S) protein of a non-fusogenic murine coronavirus, MHV-2, was compared to that of a variant, MHV-2f, with fusion activity. Two amino acids differed between The S proteins of these viruses; one was located in the signal sequence (amino acid 12) and the other in the putative cleavage site (amino acid 757). To determine which one of these amino acid changes is important for the alteration of fusogenicity, chimeric S proteins between MHV-2 and -2f were constructed and expressed in DBT cells by a vaccinia virus expression system. The results revealed that one amino acid change (Ser to Arg) at position 757 is responsible for the acquisition of fusogenicity of the MHV-2f S protein. This change also altered the susceptibility to proteolytic cleavage of the MHV-2 S protein which was originally uncleavable. We concluded that the non-fusogenic activity of MHV-2 results from the lack of cleavage of its S protein.
将一种非融合性小鼠冠状病毒MHV - 2的刺突(S)蛋白与具有融合活性的变体MHV - 2f的刺突蛋白进行了比较。这两种病毒的S蛋白之间有两个氨基酸不同;一个位于信号序列(第12位氨基酸),另一个位于假定的裂解位点(第757位氨基酸)。为了确定这些氨基酸变化中的哪一个对融合性的改变至关重要,构建了MHV - 2和 - 2f之间的嵌合S蛋白,并通过痘苗病毒表达系统在DBT细胞中进行表达。结果显示,第757位的一个氨基酸变化(丝氨酸变为精氨酸)导致了MHV - 2f S蛋白获得融合性。这种变化还改变了原本不可裂解的MHV - 2 S蛋白对蛋白水解裂解的敏感性。我们得出结论,MHV - 2的非融合活性是由于其S蛋白缺乏裂解所致。