論文

査読有り 国際誌
2019年5月28日

Establishment and Characterization of a New Cell Line Permissive for Hepatitis C Virus Infection.

Scientific reports
  • Hitoshi Omura
  • ,
  • Fanwei Liu
  • ,
  • Tetsuro Shimakami
  • ,
  • Kazuhisa Murai
  • ,
  • Takayoshi Shirasaki
  • ,
  • Juria Kitabayashi
  • ,
  • Masaya Funaki
  • ,
  • Tomoki Nishikawa
  • ,
  • Ryotaro Nakai
  • ,
  • Ariunaa Sumiyadorj
  • ,
  • Takehiro Hayashi
  • ,
  • Taro Yamashita
  • ,
  • Masao Honda
  • ,
  • Shuichi Kaneko

9
1
開始ページ
7943
終了ページ
7943
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41598-019-44257-5

Hepatitis C virus (HCV) cell culture systems have facilitated the development of efficient direct-acting antivirals against HCV. Huh-7.5, a subline of the human hepatoma cell line Huh-7, has been used widely to amplify HCV because HCV can efficiently replicate in these cells due to a defect in innate antiviral signalling. Recently, we established a novel cell line, KH, derived from human hepatocellular carcinoma, which showed atypical uptake of gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) in a Gd-EOB-DTPA-enhanced magnetic resonance imaging study. KH cells expressed hepatocyte markers including microRNA-122 (miR-122) at a lower level than Huh-7.5 cells. We demonstrated that KH cells could support the entire life cycle of HCV; however, HCV replicated at a lower rate in KH cells compared to Huh-7.5 cells, and virus particles produced from KH cells seemed to have some disadvantages in viral assembly compared with those produced from Huh-7.5 cells. KH cells had more robust interferon-stimulated gene expression and induction upon HCV RNA transfection, interferon-α2b addition, and HCV infection than Huh-7.5 cells. Interestingly, both miR-122 supplementation and IRF3 knockout in KH cells boosted HCV replication to a similar level as in Huh-7.5 cells, suggesting that intact innate antiviral signalling and lower miR-122 expression limit HCV replication in KH cells. KH cells will enable a deeper understanding of the role of the innate immune response in persistent HCV infection.

リンク情報
DOI
https://doi.org/10.1038/s41598-019-44257-5
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31138826
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6538753

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