Study | Transcription factor | Effect of HCV |
---|---|---|
Waris G et al. [69] | SREBP-precursor (Sterol response element binding protein) | HCV-2 infection leads to activation of three isoforms of SREBPs (forms 1, 1c and 2). Moreover NS4B and core protein of genotype 3 activates SREBPs through proteolytic cleavage. |
Qadri I et al. [70] | HNF1 and HNF4 (hepatocyte nuclear factor) | Increased expression of HNF1 and HFN4 mRNA in HCV subgenomic replicon-expressing Huh.8 cells. The ability of HCV to induce HNF1 and HNF4 is attributed to 1) increased oxidative stress and 2) direct protein-protein interactions between HCV non-structural component (NS) 5A and HNF1, leading to enhanced HNF1 DNA binding. |
Yamaguchi A et al. [71] | PPAR-α (peroxisome proliferator-activated receptor) | In HCV core protein-expressing mice PPAR-α was down-regulated |
Kim KH et al. [72] | PPAR-γ | The NS5A increases the transcriptional activity and gene expression of PPARγ |
Tsutsumi T et al. [73] Yamaguchi A et al [71] | RXRα (retinoid X receptor alpha) | HCV-Core binds to and activates RXRα |
Tanaka N et al. [74] | PPAR-α, | Persistent PPARα activation is essential for development of severe hepatic steatosis and its progression into hepatocellular carcinoma in the liver of core gene transgenic mice |
Dharancy et al. [75] | PPAR-α, | Reduced mRNA levels of PPAR-α in HCV infected patients and in HCV core-expressing HepG2 cells |