Alcohol consumption exacerbates the pathogenesis of hepatitis C virus (HCV) infection and aggravates disease consequences in alcohol‐abusing patients. Although the exact reasons by which alcohol consumption affects several cellular pathways in liver cells are not clear, they might be partially attributed to the ability of alcohol to further suppress the innate immunity, modulation of autophagy and also its relationship with reactive oxygen species (ROS) generation. To evaluate these issues, Huh7 cells harboring HCV replicon and Cytochrome p450 (CYP2E1) plasmid were exposed to ethanol and mRNA expression of Beclin-1, interferon-stimulated gene15 (ISG15) genes and HCV NS5B for two different times were relatively quantitated. ROS was determined by flow cytometry. The results showed that alcohol treatment in a short time caused an increase in HCV NS5B and Beclin-1 mRNA and decreased ISG 15 mRNA. Long-lasting alcohol treatment increased ROS production in Huh-7 cells and HCV replication was reduced. In conclusion, acute alcohol treatment might contribute to increase HCV replication by interference in innate immunity and induction of autophagy. Chronic alcohol treatment caused oxidative stress, which disrupts autophagy and thereby increased the rate of Huh7 cell injury.

中文翻译：

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酒精诱导的氧化应激与 HCV 复制之间的串扰

饮酒会加剧丙型肝炎病毒 (HCV) 感染的发病机制，并加重酗酒患者的疾病后果。虽然饮酒影响肝细胞中几种细胞通路的确切原因尚不清楚，但它们可能部分归因于酒精进一步抑制先天免疫、调节自噬及其与活性氧 (ROS) 的关系的能力。一代。为了评估这些问题，将携带 HCV 复制子和细胞色素 p450 (CYP2E1) 质粒的 Huh7 细胞暴露于乙醇，并对两个不同时间的 Beclin-1、干扰素刺激基因 15 (ISG15) 基因和 HCV NS5B 的 mRNA 表达进行相对定量。ROS通过流式细胞术测定。结果表明，短时间内酒精处理导致HCV NS5B和Beclin-1 mRNA增加，ISG 15 mRNA降低。长期酒精治疗增加了 Huh-7 细胞中 ROS 的产生，并减少了 HCV 的复制。总之，急性酒精治疗可能通过干扰先天免疫​​和诱导自噬来增加 HCV 复制。慢性酒精治疗会引起氧化应激，从而破坏自噬，从而增加 Huh7 细胞损伤的速度。