Interaction of the hepatitis C virus (HCV) core with cellular genes in the development of HCV-induced steatosis.
Hepatitis C virus (HCV) has chronically infected a large number of patients, leading to the development of steatosis, cirrhosis and, ultimately, hepatocellular carcinoma. The pathogenesis of HCV has not been fully explained, although steatosis is considered to contribute greatly to liver fibrosis progression, modulating host-cell lipid metabolism. Suspected underlying molecular mechanisms include interactions between HCV proteins and intracellular lipid metabolic pathways. Recent studies have suggested that the nucleocapsid of HCV (core) acts as a pathogenic factor involved in lipid droplet accumulation, changes in lipogenic gene expression and/or the activity of lipogenic proteins in a genotype-specific manner. In this review, we have tried to summarize the current knowledge regarding HCV-induced steatosis and the regulation of expression of host genes and receptors that aid in the viral life cycle and promote liver diseases.
Khan
Mahwish
M
Centre of Excellence in Molecular Biology, University of the Punjab, Lahore, Pakistan.
Jahan
Shah
S
Khaliq
Saba
S
Ijaz
Bushra
B
Ahmad
Waqar
W
Samreen
Baila
B
Hassan
Sajida
S
D005234:Fatty Liver / Q000378:metabolism* / Q000473:pathology / Q000821:virology*; D015967:Gene Expression Regulation, Viral; D016174:Hepacivirus / Q000235:genetics* / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000378:metabolism / Q000473:pathology* / Q000821:virology*; D006801:Humans; D011110:Polymorphism, Genetic; D014758:Viral Core Proteins / Q000235:genetics / Q000378:metabolism*
D014758:Viral Core Proteins