Characterization of a pantropic variant of Sendai virus derived from a host range mutant.
Characterization of a pantropic variant of Sendai virus derived from a host range mutant.
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源自宿主范围突变体的仙台病毒泛嗜性变体的表征。
DOI：
10.1016/0042-6822(88)90601-0
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发表时间：
1988
期刊：
影响因子：
3.7
通讯作者：
Seto,JT
中科院分区：
文献类型：
--
作者：
Tashiro,M;Pritzer,E;Khoshnan,MA;Yamakawa,M;Kuroda,K;Klenk,HD;Rott,R;Seto,JT
从仙台病毒的温度敏感宿主范围突变株（ts-f1）中分离到一个变异株（F1-R）。F1-R不再是温度敏感的，但它保留了宿主范围表型。与野生型病毒不同，F1-R和ts-f1在不存在胰蛋白酶的情况下在几种细胞系中进行多个复制循环。这归因于宿主范围突变体的融合（F）糖蛋白在对野生型病毒不允许的细胞中的蛋白水解活化。在鼻内感染的小鼠中，变体F1-R引起全身感染。这通过免疫组织学和从几个器官中回收的感染性病毒显示，而野生型病毒的感染仅限于肺。这些观察结果表明，F1-R的泛嗜性是普遍存在的蛋白酶对病毒的蛋白水解激活的结果。核苷酸序列分析表明，ts-f1和F1-R与野生型病毒的不同之处在于F切割位点和F2亚基糖基化位点的突变。结果表明，这些突变是ts-f1和F1-R的F蛋白裂解能力增加的原因，因此是F1-R泛向性的重要决定因素。
A variant (F1-R) was isolated from a temperature-sensitive host range mutant (ts-f1) of Sendai virus. F1-R was no longer temperature-sensitive but it retained the host range phenotype. Unlike wild-type virus, F1-R and ts-f1 undergo multiple cycles of replication in several cell lines in the absence of trypsin. This was attributed to proteolytic activation of the fusion (F) glycoprotein of the host range mutants, in cells nonpermissive to wild-type virus. In mice infected intranasally the variant F1-R caused a generalized infection. This was shown by immunohistology and with infectious virus being recovered from several organs whereas infection with wild-type virus was restricted to the lung. These observations indicate that the pantropic property of F1-R is the result of proteolytic activation of the virus by ubiquitous proteases. Nucleotide sequence analyses revealed that ts-f1 and F1-R differed from the wild-type virus by mutations at the region of the cleavage site of F and at the glycosylation site of the F2subunit. The findings indicated that these mutations are responsible for the increased cleavability of the F protein of ts-f1 and F1-R and therefore are important determinants for the pantropism of F1-R.