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Human platelet antigens polymorphisms; association to the development of liver fibrosis in patients with chronic hepatitis C.

Authors
  • Ghasemi, Ali1
  • Zadsar, Maryam2
  • Shaiegan, Mojgan3
  • Samiei, Shahram4
  • Namvar, Ali5
  • Rasouli, Mahboobeh6
  • Moosanejad, Molood7
  • 1 Department of Hematology, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran. , (Iran)
  • 2 Department of Microbiology, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran. , (Iran)
  • 3 Department of Immunohematology, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran. , (Iran)
  • 4 Department of Biochemistry, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran. , (Iran)
  • 5 Department of Genetics, Iranian Comprehensive Hemophilia Care Center, Tehran, Iran. , (Iran)
  • 6 Department of Biostatics, School of Public Health, Iran University of Medical Science, Tehran, Iran. , (Iran)
  • 7 Department of Clinical Consult, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran. , (Iran)
Type
Published Article
Journal
Journal of Medical Virology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Jan 01, 2020
Volume
92
Issue
1
Pages
45–52
Identifiers
DOI: 10.1002/jmv.25423
PMID: 30729550
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Recently, human platelet antigens (HPAs) polymorphisms are found to play a role in susceptibility to hepatitis C virus (HCV) infection and fibrosis progression. The aim of the current study was to evaluate the possible association between the HPAs polymorphisms with liver fibrosis progression in HCV patients. HPAs polymorphisms genotyping was performed in HCV patients (n = 71) by Sequence-specific primers-polymerase chain reaction. Fibrosis progression was evaluated using the Metavir scoring system and liver biopsy, and the patients were assigned to two groups, namely, G1 (n = 35) that included patients with F1 (portal fibrosis without septa) or F2 (few septa) and G2 (n = 36) that comprised patients with F3 (numerous septa) or F4 (cirrhosis). The data analyses were performed using Pearson's χ2 test. The genotype frequency of HPA-3ab was significantly higher in G1 patients than in G2 patients (P = 0.015). No statistically significant differences were found between the patient groups (G1 and G2) regarding the distributions of the allelic and genotypic frequencies of the HPA-1, -2, -4, -5, and -15 systems. Multivariate logistic regression showed an independent association between the genotype HPA-3aa/BB and severe fibrosis (F3-F4), when compared with genotype HPA-3ab, independent of the viral genotype, high alanine transaminase, sex, age, time of infection, diabetes, and high cholesterol as risk factors. The present study suggested that the HPA-3ab genotype could be noticed as a potential protecting factor against hepatic fibrosis. Therefore, the antigenic variation of integrins might be considered as a part of the coordinated inflammatory process involved in the progression of liver fibrosis. © 2019 Wiley Periodicals, Inc.

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