Bharaj IS, Singh G, Brar AS, Kacheria A, Kahlon J, Mohmand B, Sohal A, Yeneneh BT. Hepatitis C virus-associated cardiomyopathy: A review of pathogenesis. World J Virol 2025; 14(3): 108754 [DOI: 10.5501/wjv.v14.i3.108754]
Corresponding Author of This Article
Aalam Sohal, Department of Gastroenterology and Hepatology, Creighton University School of Medicine, 3216 NE 45th Pl Suite 212, Phoenix, AZ 85012, United States. aalamsohal@gmail.com
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Systematic Reviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Inderjeet Singh Bharaj, Aayushi Kacheria, Jasraj Kahlon, Department of Internal Medicine, Abrazo Health Network, Glendale, AZ 85308, United States
Gurkaranvir Singh, Department of Internal Medicine, Creighton University School of Medicine, Phoenix, AZ 85012, United States
Ajit Singh Brar, Department of Internal Medicine, Michigan State University at Hurley Medical Center, Flint, MI 48503, United States
Billal Mohmand, Beeletsega T Yeneneh, Department of Cardiology, University of Arizona Banner University Medical Center, Phoenix, AZ 85006, United States
Aalam Sohal, Department of Gastroenterology and Hepatology, Creighton University School of Medicine, Phoenix, AZ 85012, United States
Co-first authors: Inderjeet Singh Bharaj and Gurkaranvir Singh.
Author contributions: Bharaj I, Singh G, and Sohal A conceptualized and designed the study; Bharaj I, Singh G, Brar A, Kacheria A, Kahlon J, and Mohmand B conducted the literature review, interpreted the data, created the artwork, and drafted the original manuscript; Bharaj I, Singh G, Sohal A, and Yeneneh B supervised the study and made critical revisions.
Conflict-of-interest statement: All authors declare no conflict of interest to disclose.
PRISMA 2009 Checklist statement: The authors have read the PRISMA 2009 Checklist, and the manuscript was prepared and revised according to the PRISMA 2009 Check-list.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Aalam Sohal, Department of Gastroenterology and Hepatology, Creighton University School of Medicine, 3216 NE 45th Pl Suite 212, Phoenix, AZ 85012, United States. aalamsohal@gmail.com
Received: April 22, 2025 Revised: June 10, 2025 Accepted: August 27, 2025 Published online: September 25, 2025 Processing time: 156 Days and 4.9 Hours
Core Tip
Core Tip: Chronic hepatitis C virus (HCV) infection is emerging as a significant contributor to cardiomyopathy, including dilated, hypertrophic, and arrhythmogenic subtypes. This review synthesizes evidence outlining complex pathogenic mechanisms: Direct viral toxicity via HCV core protein-mediated cytokine release (e.g., tumor necrosis factor alpha), immune-mediated damage, genetic predispositions, apoptotic pathways, and cirrhotic cardiomyopathy from HCV-induced liver disease. Notably, direct-acting antiviral (DAA) therapies not only achieve high cure rates but also improve cardiac function, although potential cardiotoxic effects require vigilance. The study underscores the need for further research into mechanistic insights, biomarker validation, and expansion of global DAA access to mitigate cardiovascular risks and improve patient outcomes.
