Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein
Inhibition of the interferon-inducible protein kinase PKR by HCV E2 protein
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DOI：
10.1126/science.285.5424.107
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发表时间：
1999-07-02
期刊：
影响因子：
56.9
通讯作者：
Lai, MMC
中科院分区：
文献类型：
--
作者：
Taylor, DR;Shi, ST;Lai, MMC
大多数丙型肝炎病毒(HCV)感染的分离株对干扰素具有耐药性，干扰素是唯一可用的治疗方法，但这种耐药性的机制尚未确定。结果表明，丙型肝炎病毒包膜蛋白E2含有一个与干扰素诱导蛋白激酶PKR和翻译起始因子eIF2α(PKR靶标)的磷酸化位点相同的序列。E_2抑制PKR的激酶活性，阻断其对蛋白质合成和细胞生长的抑制作用。这种E2和PKR的相互作用可能是丙型肝炎病毒绕过干扰素抗病毒作用的机制之一。
Most isolates of hepatitis C virus (HCV) infections are resistant to interferon, the only available therapy, but the mechanism underlying this resistance has not been defined. Here it is shown that the HCV envelope protein E2 contains a sequence identical with phosphorylation sites of the interferon-inducible protein kinase PKR and the translation initiation factor eIF2 alpha, a target of PKR. E2 inhibited the kinase activity of PKR and blocked its inhibitory effect on protein synthesis and cell growth. This interaction of E2 and PKR may be one mechanism by which HCV circumvents the antiviral effect of interferon.