Related Experiment Video
Updated: Apr 28, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
Published on: July 18, 2025
Myeloperoxidase gene polymorphism predicts fibrosis severity in women with hepatitis C
Rodrigo Feliciano do Carmo1, Luydson Richardson Silva Vasconcelos2, Taciana Furtado Mendonça3
1Colegiado de Ciências Farmacêuticas, Universidade Federal do Vale do São Francisco, Pernambuco, Brazil; Rede Nordeste de Biotecnologia, Pernambuco, Brazil.
Abstract:
Oxidative stress plays an important role on liver fibrosis progression in the course of hepatitis C virus (HCV) infection. Myeloperoxidase (MPO) is an enzyme released by neutrophils and macrophages, responsible for generating hypochlorous acid and reactive oxygen species (ROS) that may lead to liver injury in HCV infection. On the other hand, antioxidant enzymes such as manganese superoxide dismutase (SOD) controls ROS-mediated damage. The aim of the present study was to investigate the influence of MPO G-463A and SOD2 Ala16Val polymorphisms in the severity of liver fibrosis in individuals with chronic HCV infection. The present study included 270 patients with chronic HCV recruited from the Gastrohepatology Service of the Oswaldo Cruz University Hospital/Liver Institute of Pernambuco (Recife, Northeastern Brazil). All patients underwent liver biopsy, which was classified according METAVIR score. The SNPs were determined by real-time PCR. After multivariate analysis adjustment, the GG genotype of MPO and the presence of metabolic syndrome were independently associated with fibrosis severity in women (P = 0.025 OR 2.25 CI 1.10-4.59 and P = 0.032 OR 2.32 CI 1.07-5.01, respectively). The presence of the GG genotype seems to be a risk factor for fibrosis severity in women with HCV.
Insights
The MPO GG genotype is a risk factor for liver fibrosis severity in women with Hepatitis C virus (HCV) infection. Metabolic syndrome also independently predicts fibrosis severity in this demographic.
Area of Science:
- Hepatology
- Genetics
- Immunology
Background:
- Oxidative stress significantly impacts liver fibrosis progression in Hepatitis C virus (HCV) infection.
- Myeloperoxidase (MPO) generates reactive oxygen species (ROS) contributing to liver injury, while manganese superoxide dismutase (SOD) mitigates ROS damage.
Purpose of the Study:
- To investigate the association between MPO G-463A and SOD2 Ala16Val gene polymorphisms and liver fibrosis severity in chronic HCV patients.
- To identify genetic and clinical factors influencing liver fibrosis progression in HCV infection.
Main Methods:
- Study included 270 chronic HCV patients from Northeastern Brazil, assessed via liver biopsy using the METAVIR score.
- Single nucleotide polymorphisms (SNPs) were genotyped using real-time PCR.
- Multivariate analysis was employed to adjust for confounding factors.
Main Results:
- The MPO GG genotype was independently associated with increased liver fibrosis severity in women (P = 0.025, OR 2.25).
- Metabolic syndrome was also independently linked to fibrosis severity in women (P = 0.032, OR 2.32).
- The GG genotype of MPO appears to be a significant risk factor for fibrosis severity specifically in women with HCV.
Conclusions:
- Genetic variations in MPO, specifically the GG genotype, are linked to more severe liver fibrosis in women with chronic HCV.
- Metabolic syndrome is an independent predictor of fibrosis severity in women with HCV.
- These findings highlight potential genetic and clinical markers for assessing fibrosis risk in HCV patients, particularly women.
Related Concept Videos
Pharmacogenetics of Phase I Enzymes: Cytochrome P450 Isozymes
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test
Pharmacogenetics of Drug Metabolism: Overview
Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow

