RNA-dependent protein kinase is required for alpha-1 interferon transgene-induced resistance to genital herpes simplex virus type 2

RNA-dependent protein kinase is required for alpha-1 interferon transgene-induced resistance to genital herpes simplex virus type 2
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DOI:
10.1128/jvi.79.14.9341-9345.2005
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发表时间:
2005-07-01
影响因子:
5.4
通讯作者:
Williams, BRG
Williams, BRG
中科院分区:
医学2区
文献类型:
--
作者:
Carr, DJJ;Tomanek, L;Williams, BRG

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我们研究了转染鼠 α-1 干扰素 (IFN-α 1) 转基因的小鼠对 2 型生殖器单纯疱疹病毒 (HSV-2) 感染的抵抗机制。用 IFN-α1 转基因原位转染小鼠导致阴道组织中 IFN 响应基因、RNA 依赖性蛋白激酶 (PKR) 升高,但不升高 2',5'-寡腺苷酸合成酶 (OAS)。与野生型小鼠或缺乏功能性 OAS 途径的小鼠相比,缺乏功能性 PKR 途径的小鼠在转染 IFN-α1 转基因后不再对生殖器 HSV-2 感染具有抵抗力,这些结果表明 PKR 是由 IFN-α1 转基因激活的主要抗病毒途径。
We investigated the mechanism of resistance to genital herpes simplex virus type 2 (HSV-2) infection in mice transfected with the murine alpha-1 interferon (IFN-alpha 1) transgene. In situ transfection of mice with the IFN-alpha 1 transgene resulted in an elevation in an IFN-responsive gene, RNA-dependent protein kinase (PKR), but not 2 ',5 '-oligoadenylate synthetases (OAS), in vaginal tissue. Coupled with the finding that mice lacking a functional PKR pathway were no longer resistant to genital HSV-2 infection following transfection with the IFN-alpha 1 transgene in comparison to wild-type mice or mice lacking a functional OAS pathway, these results suggest that PKR is the dominant antiviral pathway activated by the IFN-alpha 1 transgene.