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仙台病毒突变体TSrev-58对小鼠的肺致病性与胰蛋白酶在体外的激活作用有关。

Pneumopathogenicity in mice of a Sendai virus mutant, TSrev-58, is accompanied by in vitro activation with trypsin.

作者信息

Mochizuki Y, Tashiro M, Homma M

机构信息

Department of Microbiology, Kobe University School of Medicine, Japan.

出版信息

J Virol. 1988 Aug;62(8):3040-2. doi: 10.1128/JVI.62.8.3040-3042.1988.

Abstract

The pneumopathogenicity of a trypsin-sensitive revertant of Sendai virus, TSrev-58, which was derived from a trypsin-resistant mutant, TR-5, was examined in mice. In comparison with TR-5, the revertant had a single amino acid substitution at residue 116 (Ile----Arg) on F protein, which was the cleavage site, and had the same trypsin sensitivity as the wild-type virus. However, TSrev-58 still had a single amino acid difference from the wild-type virus at residue 109 (Asn----Asp) (M. Itoh, H. Shibuta, and M. Homma, J. Gen. Virol. 68:2939-2943, 1987). Nevertheless, the present study revealed that TSrev-58 had the same pneumopathogenicity in mice as the wild-type virus. This result indicates that the activating protease of Sendai virus present in the lungs of mice is quite similar to trypsin and also that the in vitro trypsin sensitivity of Sendai virus can be a good marker of pneumopathogenicity in mice.

摘要

对从抗胰蛋白酶突变体TR-5衍生而来的仙台病毒胰蛋白酶敏感回复株TSrev-58的肺致病性在小鼠中进行了检测。与TR-5相比,该回复株在F蛋白(裂解位点)的第116位残基处有一个氨基酸取代(异亮氨酸→精氨酸),并且具有与野生型病毒相同的胰蛋白酶敏感性。然而,TSrev-58在第109位残基处(天冬酰胺→天冬氨酸)与野生型病毒仍有一个氨基酸差异(M. 伊藤、H. 柴田和M. 本间,《普通病毒学杂志》68:2939 - 2943, 1987)。尽管如此,本研究表明TSrev-58在小鼠中的肺致病性与野生型病毒相同。这一结果表明,存在于小鼠肺中的仙台病毒激活蛋白酶与胰蛋白酶非常相似,并且仙台病毒的体外胰蛋白酶敏感性可以作为其在小鼠中肺致病性的一个良好指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad02/253745/56364d0998da/jvirol00087-0524-a.jpg

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