Immunologic, metabolic and genetic factors in hepatitis C virus infection

Table 1 Genes and hepatitis C infection

Lipid metabolism genes altered by HCV
Gene	Protein	Effect
SREBP	Sterol regulatory element-binding protein	Core protein increases the gene expression[110]
PPARα	Peroxisome proliferators-activated receptor alpha	HCV infection led to reduction in gene expression[126]
MTP	Microsomal triacylglycerol transfer protein	Core protein led to reduction in MTP activity and lower gene expression[127,128]
PEPCK	Phosphoenolpyruvate carboxykinase	NS5A increases gene expression and development of steatosis[129]
FAS	Fatty acid synthase	Core protein induces FAS promoter activity and severity of steatosis[115]
RXRα	Retinoid X receptor-alpha	Core protein enhances the transcriptional activity and contributes to the pathogenesis of infection[112]
APOE	Apolipoprotein E	HCV forms lipoviroparticles and hijacks ApoE for entry into hepatocyte[48]
Genes associated with spontaneous clearance of HCV
Gene	Protein	Allele
IL28B	Interleukin 28B	rs12979860 CC[130]
IL28B	Interleukin 28B	rs8099917 TT[131]
IL28B	Interleukin 28B	ss469415590DG[132]
KIR	Natural killer cell immunoglobulin-like receptor	KIR3DS1[133]
TNFα	Tumor necrosis factor-α	-863CC[134]
APOB	Apolipoprotein B	rs934197 TT[135]

MTP: Microsomal triacylglycerol transfer protein; FAS: Fatty acid synthase; HCV: Hepatitis C virus; SREBP: Sterol regulatory element-binding protein; PPARα: Peroxisome proliferator-activated receptor alpha; RXRα: Retinoid X receptor alpha.