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Hepatitis C Virus E2 Protein Induces Upregulation of IL-8 Pathways and Production of Heat Shock Proteins in Human Thyroid Cells

机译:丙型肝炎病毒E2蛋白诱导人甲状腺细胞中IL-8通路的上调和热休克蛋白的产生

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AbstractContext:Thyroiditis is one of the most common extrahepatic manifestations of hepatitis C virus (HCV) infection. By binding to surface cell receptor CD81, HCV envelope glycoprotein E2 mediates entry of HCV into cells. Studies have shown that different viral proteins may individually induce host responses to infection. We hypothesized that HCV E2 protein binding to CD81 expressed on thyroid cells activates a cascade of inflammatory responses that can trigger autoimmune thyroiditis in susceptible individuals.
机译:摘要背景:甲状腺炎是丙型肝炎病毒(HCV)感染的最常见肝外表现之一。通过与表面细胞受体CD81结合,HCV包膜糖蛋白E2介导HCV进入细胞。研究表明,不同的病毒蛋白可以单独诱导宿主对感染的反应。我们假设,HCV E2蛋白与甲状腺细胞上表达的CD81结合会激活一系列炎症反应,从而触发易感人群的自身免疫性甲状腺炎。

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