赛氏疱疹病毒的白细胞介素-17基因
The interleukin-17 gene of herpesvirus saimiri.
作者信息
Knappe A, Hiller C, Niphuis H, Fossiez F, Thurau M, Wittmann S, Kuhn E M, Lebecque S, Banchereau J, Rosenwirth B, Fleckenstein B, Heeney J, Fickenscher H
机构信息
Institut für Klinische und Molekulare Virologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany.
出版信息
J Virol. 1998 Jul;72(7):5797-801. doi: 10.1128/JVI.72.7.5797-5801.1998.
Abstract
In comparison to wild-type herpesvirus saimiri, viral interleukin-17 gene knockout mutants have unaltered behavior regarding viral replication, T-cell transformation in vitro, and pathogenicity in cottontop tamarins. Thus, this gene is not required for T-cell lymphoma induction but may contribute to apathogenic viral persistence in the natural host, the squirrel monkey.
摘要
与野生型赛米利疱疹病毒相比，病毒白细胞介素-17基因敲除突变体在病毒复制、体外T细胞转化以及在棉顶狨猴中的致病性方面表现未变。因此，该基因对于诱导T细胞淋巴瘤并非必需，但可能有助于病毒在天然宿主松鼠猴中无致病性地持续存在。
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本文引用的文献
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T-cell lymphoma caused by herpesvirus saimiri C488 independently of ie14/vsag, a viral gene with superantigen homology.由赛米利疱疹病毒C488独立引发的T细胞淋巴瘤，与ie14/vsag无关，ie14/vsag是一种具有超抗原同源性的病毒基因。
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Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor.松鼠猴疱疹病毒编码一种新的细胞因子IL-17，它可与一种新型细胞因子受体结合。
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