ArticleClinical and experimental immunology2007
Severe fibrosis in hepatitis C virus-infected patients is associated with increased activity of the mannan-binding lectin (MBL)/MBL-associated serine protease 1 (MASP-1) complex.
Article in Clinical and experimental immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 51 citations in OpenAlex.
- COLEC10 and COLEC11 are new serum biomarkers of chronic liver disease.European journal of medical research · 2026Article
- Host Regulators of Liver Fibrosis During Human Schistosomiasis.Frontiers in immunology · 2018Review
- AmpliSeq Screening of Genes Encoding the C-Type Lectin Receptors and Their Signaling Components Reveals a Common Variant inFrontiers in immunology · 2018Article
- HBV Viral Load and Liver Enzyme Levels May Be Associated with the WildMediators of inflammation · 2017Article
- MBL-associated serine proteases (MASPs) and infectious diseases.Molecular immunology · 2015Review
- Serum ficolin-2 concentrations are significantly changed in patients with hepatitis B virus infection and liver diseases.Virologica Sinica · 2015Article
- Serum Inter-Alpha-Trypsin Inhibitor Heavy Chain 4 (ITIH4) in Children with Chronic Hepatitis C: Relation to Liver Fibrosis and Viremia.Hepatitis research and treatment · 2014Article
- Mannan binding lectin-associated serine protease 1 is induced by hepatitis C virus infection and activates human hepatic stellate cells.Clinical and experimental immunology · 2013Article
- Serum complement C4a and its relation to liver fibrosis in children with chronic hepatitis C.World journal of hepatology · 2013Article
- Serum mannan-binding lectin in egyptian patients with chronic hepatitis C: its relation to disease progression and response to treatment.Hepatitis monthly · 2012Article
- Review
- Specific interaction of hepatitis C virus glycoproteins with mannan binding lectin inhibits virus entry.Protein & cell · 2010Article
- Gene expression profiling indicates the roles of host oxidative stress, apoptosis, lipid metabolism, and intracellular transport genes in the replication of hepatitis C virus.Journal of virology · 2010Article
- Mannose-binding lectin MBL2 gene polymorphisms and outcome of hepatitis C virus-infected patients.Journal of clinical immunology · 2008Article
- Mannan-binding lectin MBL2 gene polymorphism in chronic hepatitis C: association with the severity of liver fibrosis and response to interferon therapy.Clinical and experimental immunology · 2008Article
- Hepatitis C Virus-related Mixed Cryoglobulinemia: Pathogenesis, Clinica Manifestations, and New Therapies.Gastroenterology & hepatology · 2007Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mannan-binding lectin (MBL) binds microorganisms via interactions with glycans on the target surface. Bound MBL subsequently activates MBL-associated serine protease proenzymes (MASPs). A role for MBL in hepatitis C virus (HCV) infection had been indicated by previous studies examining MBL levels and polymorphisms in relation to disease progression and response to treatment. We undertook this study to investigate a possible relationship between disease progression and functional MBL/MASP-1 complex activity. A functional assay for MBL/MASP-1 complex activity was employed to examine serum samples from patients with chronic HCV infection, non-HCV liver disease and healthy controls. Intrapatient consistency of MBL/MASP-1 complex activity levels was assessed in sequential samples from a subgroup of patients. Median values of MBL/MASP-1 complex activity were higher in sera from patients with liver disease compared with healthy controls. MBL/MASP-1 complex activity levels correlate with severity of fibrosis after adjusting for confounding factors (P = 0.003). MBL/MASP-1 complex activity was associated more significantly with fibrosis than was MBL concentration. The potential role of MBL/MASP-1 complex activity in disease progression is worthy of further study to investigate possible mechanistic links.
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