核酸诱导的慢性病毒性肝病信号转导

StephenW

Nucleic Acid-Induced Signaling in Chronic Viral Liver Disease
Armando Andres Roca Suarez  1   2   3   4 , Barbara Testoni  3   4 , Thomas F Baumert  1   2   5   6 , Joachim Lupberger  1   2
Affiliations
Affiliations

    1
    INSERM, U1110, Institut de Recherche sur les Maladies Virales et Hépatiques, Strasbourg, France.
    2
    Université de Strasbourg, Strasbourg, France.
    3
    INSERM U1052, CNRS UMR-5286, Cancer Research Center of Lyon (CRCL), Lyon, France.
    4
    University of Lyon, Université Claude-Bernard (UCBL), Lyon, France.
    5
    Institut Hospitalo-Universitaire, Pôle Hépato-digestif, Nouvel Hôpital Civil, Strasbourg, France.
    6
    Institut Universitaire de France (IUF), Paris, France.

    PMID: 33613561 PMCID: PMC7892431 DOI: 10.3389/fimmu.2020.624034

Abstract

A hallmark for the development and progression of chronic liver diseases is the persistent dysregulation of signaling pathways related to inflammatory responses, which eventually promotes the development of hepatic fibrosis, cirrhosis and hepatocellular carcinoma (HCC). The two major etiological agents associated with these complications in immunocompetent patients are hepatitis B virus (HBV) and hepatitis C virus (HCV), accounting for almost 1.4 million liver disease-associated deaths worldwide. Although both differ significantly from the point of their genomes and viral life cycles, they exert not only individual but also common strategies to divert innate antiviral defenses. Multiple virus-modulated pathways implicated in stress and inflammation illustrate how chronic viral hepatitis persistently tweaks host signaling processes with important consequences for liver pathogenesis. The following review aims to summarize the molecular events implicated in the sensing of viral nucleic acids, the mechanisms employed by HBV and HCV to counter these measures and how the dysregulation of these cellular pathways drives the development of chronic liver disease and the progression toward HCC.

Keywords: hepatitis B virus; hepatitis C virus; hepatocellular carcinoma; inflammation; signaling; viral sensing.

Copyright © 2021 Roca Suarez, Testoni, Baumert and Lupberger.

StephenW

核酸诱导的慢性病毒性肝病信号转导
Armando Andres Roca Suarez 1 2 3 4，Barbara Testoni 3 4，Thomas F Baumert 1 2 5 6，Joachim Lupberger 1 2
隶属关系
隶属关系

    1个
    INSERM，U1110，法国斯特拉斯堡马拉维斯病毒和肝病研究所。
    2
    法国史特拉斯堡斯特拉斯堡大学。
    3
    INSERM U1052，CNRS UMR-5286，法国里昂癌症研究中心（CRCL）。
    4
    里昂大学，法国里昂大学克劳德·伯纳德大学（UCBL）。
    5
    法国史特拉斯堡的NouvelHôpitalCivil医院，Université-Universitaire，PôleHépato-digestif。
    6
    法国巴黎大学研究所（IUF），法国巴黎。

    PMID：33613561 PMCID：PMC7892431 DOI：10.3389 / fimmu.2020.624034

抽象的

慢性肝病的发生和发展的标志是与炎症反应相关的信号通路的持续失调，这最终促进了肝纤维化，肝硬化和肝细胞癌（HCC）的发展。具有免疫功能的患者中与这些并发症相关的两种主要病因是乙型肝炎病毒（HBV）和丙型肝炎病毒（HCV），约占全球与肝病相关的死亡人数约140万人。尽管两者在基因组和病毒生命周期方面都存在显着差异，但它们不仅运用个别策略，而且采用共同的策略来转移固有的抗病毒防御能力。应激和炎症牵连的多种病毒调节途径说明了慢性病毒性肝炎如何持续调节宿主信号传导过程，从而对肝脏发病机理产生重要影响。以下综述旨在总结与病毒核酸的检测有关的分子事件，HBV和HCV用来对抗这些措施的机制以及这些细胞途径的失调如何驱动慢性肝病的发展和向HCC的发展。

关键词：乙型肝炎病毒；丙型肝炎病毒；肝细胞癌；炎;发信号病毒感测。

版权所有©2021 Roca Suarez，Testoni，Baumert和Lupberger。

StephenW

https://www.frontiersin.org/arti ... mu.2020.624034/full