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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >A molecular chaperone glucose-regulated protein 94 blocks apoptosis induced by virus infection
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A molecular chaperone glucose-regulated protein 94 blocks apoptosis induced by virus infection

机译：分子伴侣葡萄糖调节蛋白94阻断病毒感染诱导的细胞凋亡

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摘要

The hepatitis C virus (HCV) E2 protein has been shown to block apoptosis and has been suggested to facilitate persistent infection of the virus. Here, we report that the anti-apoptotic activity of E2 is mediated by activation of nuclear factor kappa B (NF-kappa B) that directs expression of survival gene products such as tumor necrosis factor (TNF-alpha) receptor-associated factor 2 (TRAF2), X-chromosome-linked inhibitor of apoptosis protein (XIAP), FLICE-like inhibitory protein (FLIP), and survivin. Increased levels of these proteins were observed in HCV-infected cells and a cell line producing HCV E2 protein. The activation of NF-kappa B was mediated by HCV-E2-induced expression of the molecular chaperone glucose-regulated protein 94 (GRP94). Overexpression of GRP94 alone resulted in expression of anti-apoptotic proteins and blocked apoptosis induced by tumor-necrosis-related apoptosis-inducing ligand (TRAIL). Interestingly, increased levels of GRP94 were observed in cells supporting HCV proliferation that originated from liver tissues from HCV patients. Moreover, small interfering RNA (siRNA) knock-down of GRP94 nullified the anti-apoptotic activity of HCV E2. Conclusion: These data indicate that HCV E2 blocks apoptosis induced by HCV infection and the host immune system through overproduction of GRP94, and that HCV E2 plays an important role in persistent HCV infection.
机译：丙型肝炎病毒（HCV）E2蛋白已被证明可以阻止细胞凋亡，并被认为可以促进病毒的持续感染。在这里，我们报道E2的抗凋亡活性是由核因子κB（NF-κB）的激活介导的，该因子指导诸如肿瘤坏死因子（TNF-alpha）受体相关因子2（ TRAF2），X染色体连锁的凋亡抑制蛋白（XIAP），FLICE样抑制蛋白（FLIP）和survivin。在感染HCV的细胞和产生HCV E2蛋白的细胞系中观察到这些蛋白的水平增加。 NF-κB的激活是由HCV-E2诱导的分子伴侣葡萄糖调节蛋白94（GRP94）的表达介导的。单独的GRP94的过表达导致抗凋亡蛋白的表达，并阻断由肿瘤坏死相关凋亡诱导配体（TRAIL）诱导的凋亡。有趣的是，在支持HCV增殖的细胞中观察到GRP94的水平升高，该细胞源自HCV患者的肝脏组织。此外，GRP94的小干扰RNA（siRNA）敲除取消了HCV E2的抗凋亡活性。结论：这些数据表明，HCV E2通过过量生产GRP94阻断HCV感染和宿主免疫系统诱导的凋亡，并且HCV E2在持续性HCV感染中起重要作用。

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