Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular consequences

Authors

Mohammed Zohery, George Washington School of Medicine and Health Sciences, The George Washington University, Washington, DC 20052, United States.
Sarah Jahangir, Department of Medicine, East Carolina University/Brody School of Medicine, Greenville, NC 27834, United States.
Hamed Carter Jenna, Department of Medicine, East Carolina University/Brody School of Medicine, Greenville, NC 27834, United States.
Shiza Sarfraz, Department of Internal Medicine, East Carolina University/Brody School of Medicine, Greenville, NC 27834, United States.
Hadeera Ali, Department of Medicine, CMH Hospital, Bahawalpur 63100, Punjab, Pakistan.
Muhammad Raza, Department of Medicine, CMH Hospital, Lahore 54000, Punjab, Pakistan.
Taha Rafiq, Department of Medicine, University of Galway, Galway TK33, Ireland.
Dushyant Singh Dahiya, Division of Gastroenterology, Hepatology, and Motility, The University of Kansas School of Medicine, Kansas City, KS 66160, United States.
Vinay Jahagirdar, Department of Internal Medicine, University of Missouri-Kansas City, Kansas, MI 64110, United States.
Hassam Ali, Division of Gastroenterology, Hepatology and Nutrition, East Carolina University/Brody School of Medicine, Greenville, NC 27858, United States. hassamali155@gmail.com.

Document Type

Journal Article

Publication Date

12-25-2025

Journal

World journal of virology

Volume

14

Issue

4

DOI

10.5501/wjv.v14.i4.113217

Keywords

Cardiovascular disease; Coagulation imbalance; Cryoglobulinemia; Direct-acting antivirals; Endothelial dysfunction; Hepatitis C virus; Portal vein thrombosis; Systemic inflammation; Thrombotic risk; Venous thromboembolism

Abstract

Hepatitis C virus (HCV) infection, traditionally regarded as a hepatotropic disease, is increasingly recognized as a systemic condition with significant thrombotic implications. Chronic HCV induces a persistent proinflammatory and prothrombotic state that substantially elevates the risk of both venous and arterial events. Mechanistically, HCV drives endothelial dysfunction, enhances platelet activation, disrupts coagulation and fibrinolytic balance, and promotes immune-mediated vascular injury through cryoglobulinemia and chronic systemic inflammation. Clinical manifestations range from portal vein thrombosis and venous thromboembolism to coronary artery disease and ischemic stroke, highlighting the far-reaching consequences of virus-driven coagulopathy. Emerging evidence challenges the historical view of cirrhosis as a "naturally anticoagulated" state, instead describing a fragile hemostatic balance prone to both bleeding and thrombosis. Direct-acting antiviral therapy has transformed outcomes, not only achieving sustained virological response but also reversing systemic inflammation, improving endothelial function, and reducing thrombotic complications. However, patients with advanced fibrosis and comorbidities remain at elevated risk despite viral clearance, underscoring the need for ongoing surveillance. This minireview highlights the interplay between hepatic dysfunction, viral-induced inflammation, and cardiovascular sequelae in chronic HCV, emphasizing the importance of integrating thrombotic risk assessment into clinical care and research frameworks.

APA Citation

Zohery, Mohammed; Jahangir, Sarah; Jenna, Hamed Carter; Sarfraz, Shiza; Ali, Hadeera; Raza, Muhammad; Rafiq, Taha; Dahiya, Dushyant Singh; Jahagirdar, Vinay; and Ali, Hassam, "Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular consequences" (2025). GW Authored Works. Paper 8359.
https://hsrc.himmelfarb.gwu.edu/gwhpubs/8359

Department

School of Medicine and Health Sciences Student Works