Isegawa Y, Tanishita O, Ueda S, Yamanishi K
Department of Virology, Osaka University, Japan.
J Gen Virol. 1994 Nov;75 ( Pt 11):3273-8. doi: 10.1099/0022-1317-75-11-3273.
Hantaan virus (HV) of the genus Hantavirus causes a fatal disease in suckling mice following intraperitoneal or intracerebral infection. HV cl-1, which was obtained from the 76-118 strain of HV by growth in Vero E6 cells, exhibited high mortality rates in mice whereas mice infected with HV cl-2 survived without any clinical signs. To determine the molecular basis for the marked difference in virulence, we compared the nucleotide sequences of the large (L), medium (M) and small (S) segments of HV cl-1 genome with those of HV cl-2 and found that there was only one predicted amino acid substitution. This amino acid substitution was in position 1124 of the glycoprotein encoded by the M genome segment, in which serine in HV cl-1 was replaced by glycine in HV cl-2. Although there were several nucleotide and amino acid differences between the parental 76-118 strain and HV cl-1, the serine in position 1124 of the glycoprotein was common to the pathogenic parent and the pathogenic mutant. These results suggest that this substitution may be responsible for the virulence of this hantavirus.
汉坦病毒属的汉坦病毒（HV）在经腹腔或脑内感染后会导致乳鼠患上致命疾病。HV cl-1是通过在Vero E6细胞中培养从HV的76-118株获得的，在小鼠中表现出高死亡率，而感染HV cl-2的小鼠存活下来且没有任何临床症状。为了确定毒力显著差异的分子基础，我们将HV cl-1基因组的大（L）、中（M）和小（S）片段的核苷酸序列与HV cl-2的进行了比较，发现只有一个预测的氨基酸替换。这个氨基酸替换位于M基因组片段编码的糖蛋白的第1124位，其中HV cl-1中的丝氨酸被HV cl-2中的甘氨酸取代。尽管亲本76-118株与HV cl-1之间存在几个核苷酸和氨基酸差异，但糖蛋白第1124位的丝氨酸在致病亲本和致病突变体中是相同的。这些结果表明，这种替换可能是这种汉坦病毒毒力的原因。
