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10.3390/ijms21072583

http://scihub22266oqcxt.onion/10.3390/ijms21072583
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32276399!7177520!32276399
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suck abstract from ncbi


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pmid32276399      Int+J+Mol+Sci 2020 ; 21 (7): ä
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  • Interferon Response in Hepatitis C Virus-Infected Hepatocytes: Issues to Consider in the Era of Direct-Acting Antivirals #MMPMID32276399
  • Sung PS; Shin EC
  • Int J Mol Sci 2020[Apr]; 21 (7): ä PMID32276399show ga
  • When interferons (IFNs) bind to their receptors, they upregulate numerous IFN-stimulated genes (ISGs) with antiviral and immune regulatory activities. Hepatitis C virus (HCV) is a single-stranded, positive-sense RNA virus that affects over 71 million people in the global population. Hepatocytes infected with HCV produce types I and III IFNs. These endogenous IFNs upregulate a set of ISGs that negatively impact the outcome of pegylated IFN-alpha and ribavirin treatments, which were previously used to treat HCV. In addition, the IFNL4 genotype was the primary polymorphism responsible for a suboptimal treatment response to pegylated IFN-alpha and ribavirin. However, recently developed direct-acting antivirals have demonstrated a high rate of sustained virological response without pegylated IFN-alpha. Herein, we review recent studies on types I and III IFN responses to in HCV-infected hepatocytes. In particular, we focused on open issues related to IFN responses in the direct-acting antiviral era.
  • |*Immunity, Innate[MESH]
  • |Antiviral Agents/*pharmacology/therapeutic use[MESH]
  • |Gene Expression Regulation[MESH]
  • |Hepatitis C/*drug therapy/genetics/immunology[MESH]
  • |Hepatocytes/immunology/*metabolism[MESH]
  • |Humans[MESH]
  • |Interferon Type I/genetics[MESH]


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