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- W1978369706 abstract "Hepatitis C virus (HCV) interacts extensively with host factors to not only establish productive infection but also trigger unique pathological processes. Our recent genome-wide siRNA screen demonstrated that IjB kinase-a (IKK-a) is a crucial host factor for HCV. Here we describe a new nuclear factor jB (NF-jB)-independent and kinasemediated nuclear function of IKK-a in HCV assembly. HCV, through its 30 untranslated region, interacts with DEAD box polypeptide 3, X-linked (DDX3X) to activate IKK-a, which translocates to the nucleus and induces a CBP/p300-mediated transcriptional program involving sterol regulatory element-binding proteins (SREBPs). This innate pathway induces lipogenic genes and enhances core-associated lipid droplet formation to facilitate viral assembly. Chemical inhibitors of IKK-a suppress HCV infection and IKK-a-induced lipogenesis, offering a proof-of-concept approach for new HCV therapeutic development. Our results show that HCV uses a novel mechanism to exploit intrinsic innate responses and hijack lipid metabolism, which may contribute to high chronicity rates and the pathological hallmark of steatosis in HCV infection." @default.
- W1978369706 created "2016-06-24" @default.
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- W1978369706 date "2013-11-01" @default.
- W1978369706 modified "2023-10-18" @default.
- W1978369706 title "Hepatitis C virus co-opts innate immunity component for lipid droplet formation" @default.
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- W1978369706 doi "https://doi.org/10.1016/j.jhep.2013.07.002" @default.
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