Publication

Impact of il10, mtp, sod2, and apoe gene polymorphisms on the severity of liver fibrosis induced by hcv genotype 4

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Last modified
  • 05/14/2025
Type of Material
Authors
    Amr Ali Hemeda, Future University in EgyptAmal Ahmad Mohamed, National Hepatology and Tropical Medicine Research InstituteRamy Karam Aziz, Cairo University Faculty of PharmacyMohamed Abdel Hakeem, Emory UniversityMarwa Ali-Tammam, Future University in Egypt
Language
  • English
Date
  • 2021-04-01
Publisher
  • MDPI
Publication Version
Copyright Statement
  • © 2021 by the authors.
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Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 13
Issue
  • 4
Grant/Funding Information
  • This research received no external funding.
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Abstract
  • Complications of hepatitis C virus (HCV) chronic infection cause ~400,000 deaths world-wide annually. One complication, liver fibrosis, is influenced by host genetic factors. Genes influenc-ing fibrosis include immune, metabolic, oxidative stress, and viral entry genes, such as interleukin 10 (IL10), microsomal triglyceride-transfer protein (MTP), superoxide dismutase-2 (SOD2), and apolipoprotein E (APOE)-encoding genes, respectively. Thus, correlating variations in these genes with HCV-induced fibrosis represents an attractive biomarker for the prognosis of fibrosis severity in chronically infected patients. Here, we aimed to test whether polymorphisms in IL10, MTP, SOD2, and APOE genes correlated with the severity of fibrosis induced by HCV genotype 4 (HCV-gt4) in a cohort of chronically infected Egyptian patients. Our results demonstrate a significant association between the severity of fibrosis and specific SNPs in IL-10, SOD2, and ApoE-encoding genes. Haplotype-combination analysis for IL10, MTP, SOD2, and APOE showed statistically significant associations between specific haplotype combinations and fibrosis severity. Identifying biomark-ers correlating with the severity of HCV-gt4-induced fibrosis would significantly impact precision prophylaxis and treatment of patients at risk.
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Keywords
Research Categories
  • Biology, Genetics
  • Biology, Cell

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