Suppr超能文献

干扰素在慢性丙型肝炎感染中的作用。

Role of Interferons in Chronic Hepatitis C Infection.

作者信息

Scagnolari Carolina, Monteleone Katia, Cacciotti Giulia, Antonelli Guido

机构信息

Department of Molecular Medicine, Laboratory of Virology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia, Fondazione Cenci Bolognetti, Italy.

Department of Molecular Medicine, Laboratory of Virology, Sapienza University of Rome, Laboratory affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Viale di Porta Tiburtina 28 - 00185 Rome, Italy.

出版信息

Curr Drug Targets. 2017;18(7):844-850. doi: 10.2174/1389450117666160201112632.

Abstract

It is known that the production of and/or response to interferon (IFN) are deregulated during chronic hepatitis C virus (HCV) infection. In particular, several studies have shown that patients with chronic HCV infection who have a high natural level of IFN-stimulated genes (ISGs) do not achieve viral clearance and have a poor response to treatment with pegylated IFNα and ribavirin. The viral and/or host factors that are responsible for the higher endogenous ISGs expression in some HCV infected patients compared to others remain to be determined. However, type III IFNs, and in particular the new discovered IFN lambda (L) 4 Gene, appear to play a dominant role in driving ISGs response and in contributing to the establishment of HCV persistence. This review focuses on recent studies on how the ISGs response and the IFNλ genetic factors (interleukin-28B and IFNL4) affect the clinical outcome of HCV infection highlighting their impact in the current antiviral therapies with direct acting antiviral agents.

摘要

众所周知,在慢性丙型肝炎病毒(HCV)感染期间,干扰素(IFN)的产生和/或反应会失调。特别是,多项研究表明,慢性HCV感染患者中,天然IFN刺激基因(ISG)水平较高者无法实现病毒清除,且对聚乙二醇化IFNα和利巴韦林治疗反应不佳。与其他患者相比,导致部分HCV感染患者内源性ISG表达较高的病毒和/或宿主因素仍有待确定。然而,III型IFN,尤其是新发现的IFNλ4基因,似乎在驱动ISG反应以及导致HCV持续存在方面起主导作用。本综述重点关注近期关于ISG反应和IFNλ遗传因素(白细胞介素-28B和IFNL4)如何影响HCV感染临床结局的研究,突出它们在当前使用直接抗病毒药物的抗病毒治疗中的影响。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验