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Hepatitis C virus and atherosclerosis: A legacy after virologic cure?
M F Bassendine1, S U Nielsen2, S H Bridge3
1Institute of Cellular Medicine, Newcastle University, United Kingdom; Department of Hepatology & Gastroenterology, Imperial College London, United Kingdom.
Insights
Hepatitis C virus (HCV) infection increases cardiovascular and cerebrovascular risks, potentially via immune complexes promoting atherosclerosis. Even after cure, residual risks may persist, impacting long-term health.
Area of Science:
- Immunology
- Virology
- Cardiovascular Medicine
Background:
- Hepatitis C virus (HCV) infects over 170 million people globally.
- HCV infection is linked to increased cardiovascular and cerebrovascular mortality.
- Despite a favorable lipid profile, HCV patients show elevated atherosclerosis risk.
Purpose of the Study:
- To explore the mechanisms behind atherosclerosis development in chronic HCV.
- To hypothesize the role of immune complexes in HCV-associated atherosclerosis.
- To discuss the clinical and therapeutic implications of persistent HCV infection on cardiovascular health.
Main Methods:
- Review of epidemiological studies on HCV and cardiovascular outcomes.
- Discussion of potential pathogenetic factors in HCV-induced atherosclerosis.
- Hypothesis formulation based on immune response to viral and lipoprotein particles.
Main Results:
- HCV infection is associated with increased cardiovascular and cerebrovascular mortality.
- Atherosclerosis development may be driven by circulating immune complexes.
- HCV particles might trigger antibody responses to lipoproteins, similar to modified LDL autoantibodies.
Conclusions:
- Immune complexes forming against HCV-lipoprotein complexes are a potential mechanism for atherosclerosis in HCV.
- Virologic cure may not fully reverse atherosclerosis risk; residual risks and cholesterol increases can drive lesion progression.
- Persistent HCV infection leaves a lasting legacy on cardiovascular health with clinical implications.
Abstract:
Hepatitis C virus (HCV) is a major pathogen with approximately 3% of the world's population (over 170 million) infected. Epidemiological studies have shown HCV is associated with an increased risk of cardiovascular and cerebrovascular mortality as well as peripheral arterial disease. This is despite HCV inducing an ostensibly favourable lipid profile with accompanying low classical risk score for atherosclerosis (AS). We discuss possible factors involved in the aetiopathogenesis of atherosclerosis in chronic HCV and hypothesise that an important mechanism underlying the development of AS is the presence of circulating low-density immune complexes that induce an inflammatory response. We suggest that HCV particles may be inducing an antibody response to lipoproteins present in the lipoviral particles and sub-viral particles - a concept similar to the more general 'autoantibody' response to modified LDL. After virologic cure some AS risk factors will recede but an increase in serum cholesterol could result in progression of early atherosclerotic lesions, leaving a legacy from persistent HCV infection that has clinical and therapeutic implications.
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