Suppression of hepatitis C virus replicon by TGF-beta.
Hepatitis C virus (HCV) is one of the major causative agents of liver diseases, such as liver inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. Using an efficient HCV subgenomic replicon system, we demonstrate that transforming growth factor-beta (TGF-beta) suppresses viral RNA replication and protein expression from the HCV replicon. We further show that the anti-viral effect of this cytokine is associated with cellular growth arrest in a manner dependent on Smad signaling, not mitogen-activated protein kinase (MAPK) signaling. These results suggest a novel insight into the mechanisms of liver diseases caused by HCV.
Murata
Takayuki
T
Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.
Ohshima
Takayuki
T
Yamaji
Masashi
M
Hosaka
Masahiro
M
Miyanari
Yusuke
Y
Hijikata
Makoto
M
Shimotohno
Kunitada
K
D045744:Cell Line, Tumor; D004268:DNA-Binding Proteins / Q000378:metabolism; D016174:Hepacivirus / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D010957:Plasmids / Q000235:genetics; D012093:Replicon / Q000187:drug effects*; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D014779:Virus Replication
D004268:DNA-Binding Proteins; D016212:Transforming Growth Factor beta