Department of Hematology, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran.
Department of Microbiology, Blood Transfusion Research Center, High Institute for Research & Education in Transfusion Medicine, Tehran, Iran.
J Med Virol. 2020 Jan;92(1):45-52. doi: 10.1002/jmv.25423. Epub 2019 Oct 9.
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 χ 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.
最近，人类血小板抗原（HPAs）多态性被发现与丙型肝炎病毒（HCV）感染易感性和纤维化进展有关。本研究旨在评估 HPAs 多态性与 HCV 患者肝纤维化进展之间的可能相关性。采用序列特异性引物聚合酶链反应（PCR）对 HCV 患者（n=71）的 HPAs 多态性进行基因分型。采用 Metavir 评分系统和肝活检评估纤维化进展，将患者分为两组，即 G1 组（n=35），包括 F1（无间隔的门脉纤维化）或 F2（少量间隔）患者；G2 组（n=36），包括 F3（大量间隔）或 F4（肝硬化）患者。数据分析采用 Pearson χ检验。G1 组患者的 HPA-3ab 基因型频率明显高于 G2 组（P=0.015）。两组患者（G1 和 G2）在 HPA-1、-2、-4、-5 和-15 系统的等位基因和基因型频率分布方面无统计学差异。多因素 logistic 回归显示，与基因型 HPA-3ab 相比，基因型 HPA-3aa/BB 与严重纤维化（F3-F4）独立相关，而与病毒基因型、高丙氨酸转氨酶、性别、年龄、感染时间、糖尿病和高胆固醇等危险因素无关。本研究表明，HPA-3ab 基因型可能是肝纤维化的潜在保护因素。因此，整合素的抗原变异可能被认为是参与肝纤维化进展的炎症反应协调过程的一部分。
