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Published on: November 27, 2019
Complement activation correlates with liver necrosis and fibrosis in chronic hepatitis C
Matthäus Vasel1, Renate Rutz2, Claus Bersch3
1Max-Planck Institute of Biochemistry, Martinsried, Germany; Institute of Immunology, University of Heidelberg, Germany.
Insights
Chronic hepatitis C infection activates complement, a key part of the immune system. Complement activation predicts liver inflammation and fibrosis in patients with hepatitis C.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Chronic hepatitis C viral infection is known to modulate the complement system.
- The complement system plays a crucial role in immune responses and inflammation.
Purpose of the Study:
- To investigate whether complement system analysis can predict liver inflammation and fibrosis in patients with chronic hepatitis C.
- To assess the correlation between complement activation markers and liver disease severity.
Main Methods:
- Compared complement activity (CH50) and SC5b-9 levels in 50 chronic hepatitis C patients, 50 healthy controls, and 35 patients with other liver diseases.
- Analyzed liver biopsies for inflammation and fibrosis using the METAVIR scoring system.
- Assessed the prevalence of C1q auto-antibodies and their association with disease parameters.
Main Results:
- Total plasma complement activity (CH50) was diminished in hepatitis C patients, correlating with increased necrosis and higher METAVIR activity scores.
- The complement activation marker SC5b-9 showed significant correlations with inflammation, activity, and fibrosis scores.
- C1q auto-antibodies were more prevalent in hepatitis C patients and associated with increased inflammation and fibrosis.
Conclusions:
- Complement activation contributes to liver inflammation in chronic hepatitis C.
- Complement system analysis, including CH50, SC5b-9, and C1q auto-antibodies, serves as a valuable predictor of liver inflammation and fibrosis in chronic hepatitis C patients.
- Targeting complement pathways may offer therapeutic strategies for managing hepatitis C-related liver disease.
Abstract:
Chronic hepatitis C viral infection modulates complement. The aim of this study was to determine whether complement analysis predicts liver inflammation and fibrosis in patients with chronic hepatitis C. 50 chronic hepatitis C patients who underwent a liver biopsy were compared to 50 healthy controls and 35 patients with various liver diseases. Total plasma complement activity (CH50) in plasma was diminished in hepatitis C patients suggesting complement activation. This decrease correlated with increased necrosis (r = -0.24, p < 0.05), and patients with levels below the normal range had a higher METAVIR activity score reflecting enhanced inflammation. SC5b-9, a marker of complement activation, correlated with inflammation (r = 0.40, p < 0.05), activity (r = 0.42, p < 0.05), and fibrosis scores (r = 0.49, p < 0.05). Finally, the prevalence of C1q auto-antibodies was higher in hepatitis C patients, and their presence was associated with increased inflammation and seemed to affect fibrosis. We conclude that complement-induced liver inflammation contributes to fibrosis in patients with chronic hepatitis C.
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