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Published on: February 19, 2019
A Unified Histopathological Framework of Liver Fibrogenesis in Chronic Viral Hepatitis B, C and Coinfection
Alina Dumitrache Păunescu1,2, Nicoleta Anca Ionescu Șuțan2, Liliana Cristina Soare2
1Doctoral School, University of Medicine and Pharmacy of Craiova, Petru-Rareș Street No. 2, 200349 Craiova, Romania.
Insights
Hepatitis B and C coinfection accelerates liver disease progression. Coinfection amplifies liver injury markers, showing increased inflammation and fibrosis signaling compared to single infections.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Chronic viral hepatitis B (HBV) and C (HCV) cause progressive liver disease.
- HBV-HCV coinfection accelerates liver fibrosis and hepatocellular injury.
Purpose of the Study:
- To evaluate integrated biochemical, histopathological, and immunohistochemical features in patients with chronic hepatitis B (CHB), chronic hepatitis C (CHC), and CHB+C coinfection.
- To correlate these features with biochemical, hematological, and prognostic parameters.
Main Methods:
- Assessed liver biopsies using Ishak and METAVIR scoring systems.
- Performed immunohistochemical analysis of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), CD5L, and glial fibrillary acidic protein (GFAP) using H-score.
- Correlated findings with biochemical and hematological parameters.
Main Results:
- Coinfected patients showed significantly higher ALT, AST, and GGT levels and increased CD5L expression, indicating enhanced macrophage-associated inflammation.
- While fibrosis stages were comparable, CHB+C coinfection demonstrated an upward trend in α-SMA, TGF-β1, and GFAP, suggesting intensified profibrogenic signaling.
- Principal Component Analysis revealed distinct biochemical clusters related to hepatocellular injury, hepatic functional impairment, and lipid metabolism.
Conclusions:
- Chronic viral hepatitis presents a multidimensional pattern of liver injury.
- CHB+C coinfection amplifies profibrogenic and hepatocellular markers biochemically and histologically, worsening liver disease progression.
Background:
Chronic hepatitis B and C remain major causes of progressive liver disease, while HBV-HCV coinfection is associated with accelerated fibrosis and hepatocellular injury.
Methods:
This study evaluated integrated biochemical, histopathological, and immunohistochemical features in patients with chronic hepatitis B (CHB, n = 29), chronic hepatitis C (CHC, n = 15), and CHB+C coinfection (CHB+C, n = 10). Liver biopsies were assessed using Ishak and METAVIR scoring systems, alongside immunohistochemical analysis of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), CD5L, and glial fibrillary acidic protein (GFAP), quantified by H-score. These findings were correlated with biochemical, hematological, and prognostic parameters.
Results:
Coinfected patients exhibited significantly higher serum ALT, AST, and GGT levels (p ≤ 0.011) and increased CD5L expression (median H-score 197.5 vs. 135 in CHB, p = 0.009), indicating enhanced macrophage-associated inflammatory activity. Although fibrosis stages were comparable across groups, median H-scores for α-SMA, TGF-β1, and GFAP showed a consistent upward trend in CHB+C, suggesting intensified profibrogenic signaling. Principal Component Analysis identified distinct biochemical clusters related to hepatocellular injury, hepatic functional impairment (synthetic and excretory axis), and lipid metabolism.
Conclusions:
These findings highlight a multidimensional pattern of liver injury in chronic viral hepatitis, with CHB+C coinfection amplifying profibrogenic and hepatocellular markers, both biochemically and histologically.
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