Figure 3: Molecular genetic mechanisms of development of hepatitis C associated liver cirrhosis and hepatocellular carcinoma. Chronic infection of HCV induces hepatic cell injury, necrosis and regeneration. Activation of fibrotic cells (stellate cells, myofibroblasts and fibroblasts) will form fibrosis and thick liver cell plates which further progresses into cirrhosis. Viral proteins are responsible for the viral replication as well as malignant transformation of hepatocytes during regeneration. Genetic instability, loss of heterozygosity, aberrant copy number variation, telomere shortening, epigenetic changes, dysregulation of MicroRNAs, somatic mutations, germ line mutations and single nucleotide polymorphisms in immune genes are drivers of carcinogenesis. Host and environmental factors, such as age, immune status, comorbidity, alcohol consumption, co-infection with HBV or HIV and aflatoxin will precipitate the progression of the disease.