Hepatitis C virus (HCV) infection is caused by an enveloped, single-stranded RNA virus of the Flaviviridae family that establishes chronic infection in the majority of those exposed, making it a major global cause of cirrhosis, hepatocellular carcinoma, and liver-related mortality. Transmission occurs predominantly …
Hepatitis C virus (HCV) infection is caused by an enveloped, single-stranded RNA virus of the Flaviviridae family that establishes chronic infection in the majority of those exposed, making it a major global cause of cirrhosis, hepatocellular carcinoma, and liver-related mortality. Transmission occurs predominantly through percutaneous exposure to infected blood, and chronic infection is often clinically silent for years while progressive hepatic fibrosis develops. The therapeutic landscape has been transformed by direct-acting antiviral regimens capable of achieving sustained virologic response and cure in most patients. Research in this area examines angiogenic and inflammatory markers, including Tie2, CD14, and angiopoietin, in hepatocellular carcinoma complicating HCV infection, the burden and trends of chronic liver disease in hospital-based cohorts, and the laboratory diagnosis and seroprevalence of HCV alongside hepatitis B virus and HIV among blood donors. Related work addresses transfusion safety, co-infection, vitamin D status in chronic liver disease, and the molecular and computational study of disease-associated genetic variation. The journal publishes peer-reviewed clinical, epidemiologic, and laboratory studies addressing the transmission, diagnosis, hepatic complications, and population burden of hepatitis C virus infection and chronic liver disease in diverse settings.
12 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 12 articles above have been cited 89 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
A sample of recent works citing this journal's research on Hepatitis C Virus Infection, linking to each citing work.