Regulated expression of the interferon-induced protein kinase p68 (PKR) by vaccinia virus recombinants inhibits the replication of vesicular stomatitis virus but not that of poliovirus.
Regulated expression of the interferon-induced protein kinase p68 (PKR) by vaccinia virus recombinants inhibits the replication of vesicular stomatitis virus but not that of poliovirus.
复制标题
痘苗病毒重组体调节干扰素诱导的蛋白激酶 p68 (PKR) 的表达，抑制水泡性口炎病毒的复制，但不抑制脊髓灰质炎病毒的复制。
DOI：
10.1089/jir.1996.16.1073
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Esteban,M
中科院分区：
文献类型：
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作者：
Lee,SB;Bablanian,R;Esteban,M
干扰素诱导的人蛋白激酶p68的直接抗病毒作用仅表现为对抗脑心肌炎病毒（EMCV）和牛痘病毒（VV）。为了确定p68激酶（PKR）是否具有广泛的抗病毒作用，我们使用了表达p68激酶的VV重组体在大肠杆菌和两种RNA病毒（水泡性口炎病毒（VSV）和脊髓灰质炎病毒）的lac I操纵子/阻遏子元件的调节下的共感染。在VV重组体和VSV共感染的细胞中，用异丙基-B-D-硫代半乳糖苷（IPTG）诱导野生型p68激酶或缺乏dsRNA结合结构域的突变体导致VV和VSV蛋白合成的抑制。在用p68激酶的催化失活点突变体lys-arg 296感染的细胞中未观察到这种抑制。当细胞与VV重组体和脊髓灰质炎病毒共感染时，激活p68激酶的诱导导致VV蛋白的减少，但脊髓灰质炎病毒蛋白或脊髓灰质炎病毒产量没有减少。免疫印迹分析显示，p68激酶在混合感染过程中表达。我们的研究结果表明p68激酶对VV，VSV和脊髓灰质炎病毒复制的差异效应。我们认为，在一个特定的病毒-细胞系统中，病毒对p68激酶的不同敏感性可能是由于活性酶的水平。
A direct antiviral role of the interferon-induced human protein kinase p68 has been shown only against encephalomyocarditis virus (EMCV) and vaccinia virus (VV). To determine if p68 kinase (PKR) has a broad antiviral effect, we have used coinfections between VV recombinants expressing p68 kinase under regulation of the lac I operator/repressor elements ofEscherichia coliand two RNA viruses, vesicular stomatitis virus (VSV) and poliovirus. In cells coinfected with VV recombinants and VSV, induction with isopropyl-B-D-thiogalactoside (IPTG) of wild-type p68 kinase or a mutant lacking the dsRNA binding domain resulted in inhibition of both VV and VSV protein synthesis. This inhibition is not observed in cells infected with a catalytically inactive point mutant lys-arg296 of p68 kinase. When cells are coinfected with VV recombinants and poliovirus, induction of active p68 kinase resulted in a decrease in VV proteins but not in poliovirus proteins or poliovirus yields. Immunoblot analysis revealed that p68 kinase was expressed during mixed infections. Our results demonstrate a differential effect of p68 kinase on the replication of VV, VSV, and poliovirus. We suggest that in a particular virus-cell system, the different sensitivity of a virus to p68 kinase is probably due to levels of active enzyme.