Picelli Natália, Tanikawa Aline Aki, Grotto Rejane Maria Tommasini, Silva Giovanni Faria, Barbosa Alexandre Naime, Ferrasi Adriana Camargo, Silveira Liciana Vaz de Arruda, Pardini Maria Inês de Moura Campos
Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR.
Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR.
Rev Soc Bras Med Trop. 2015 Jul-Aug;48(4):406-9. doi: 10.1590/0037-8682-0152-2015.
Hepatic fibrosis progression in patients with chronic hepatitis C virus infections has been associated with viral and host factors, including genetic polymorphisms. Human platelet antigen polymorphisms are associated with the rapid development of fibrosis in HCV-monoinfected patients. This study aimed to determine whether such an association exists in human immunodeficiency virus-1/hepatitis C virus-coinfected patients.
Genomic deoxyribonucleic acid from 36 human immunodeficiency virus-1/hepatitis C virus-coinfected patients was genotyped to determine the presence of human platelet antigens-1, -3, or -5 polymorphisms. Fibrosis progression was evaluated using the Metavir scoring system, and the patients were assigned to two groups, namely, G1 that comprised patients with F1, portal fibrosis without septa, or F2, few septa (n = 23) and G2 that comprised patients with F3, numerous septa, or F4, cirrhosis (n = 13). Fisher's exact test was utilized to determine possible associations between the human platelet antigen polymorphisms and fibrosis progression.
There were no deviations from the Hardy-Weinberg equilibrium in the human platelet antigen systems evaluated. Statistically significant differences were not observed between G1 and G2 with respect to the distributions of the allelic and genotypic frequencies of the human platelet antigen systems.
The greater stimulation of hepatic stellate cells by the human immunodeficiency virus and, consequently, the increased expression of transforming growth factor beta can offset the effect of human platelet antigen polymorphism on the progression of fibrosis in patients coinfected with the human immunodeficiency virus-1 and the hepatitis C virus.
慢性丙型肝炎病毒感染患者的肝纤维化进展与病毒和宿主因素有关，包括基因多态性。人类血小板抗原多态性与丙型肝炎病毒单感染患者纤维化的快速发展有关。本研究旨在确定这种关联在人类免疫缺陷病毒1型/丙型肝炎病毒合并感染患者中是否存在。
对36例人类免疫缺陷病毒1型/丙型肝炎病毒合并感染患者的基因组脱氧核糖核酸进行基因分型，以确定人类血小板抗原-1、-3或-5多态性的存在。使用梅塔维评分系统评估纤维化进展，患者被分为两组，即G1组，包括F1期（无间隔的门脉纤维化）或F2期（少量间隔）的患者（n = 23）和G2组，包括F3期（大量间隔）或F4期（肝硬化）的患者（n = 13）。采用费舍尔精确检验来确定人类血小板抗原多态性与纤维化进展之间的可能关联。
在所评估的人类血小板抗原系统中，未观察到偏离哈迪-温伯格平衡的情况。在G1组和G2组之间，未观察到人类血小板抗原系统等位基因和基因型频率分布的统计学显著差异。
人类免疫缺陷病毒对肝星状细胞的更大刺激以及由此导致的转化生长因子β表达增加，可抵消人类血小板抗原多态性对人类免疫缺陷病毒1型和丙型肝炎病毒合并感染患者纤维化进展的影响。
