The absence of the human platelet antigen polymorphism effect on fibrosis progression in human immunodeficiency virus-1/hepatitis C virus coinfected patients.

Autor:	Picelli N; Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Tanikawa AA; Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Grotto RM; Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Silva GF; Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Barbosa AN; Departamento de Doenças Tropicais, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Ferrasi AC; Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Silveira LV; Departamento de Bioestatística, Instituto de Biociências de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR., Pardini MI; Laboratório de Biologia Molecular do Hemocentro, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista Júlio de Mesquita Filho, Botucatu, São Paulo, BR.
Jazyk:	angličtina
Zdroj:	Revista da Sociedade Brasileira de Medicina Tropical [Rev Soc Bras Med Trop] 2015 Jul-Aug; Vol. 48 (4), pp. 406-9.
DOI:	10.1590/0037-8682-0152-2015
Abstrakt:	Introduction: 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. Methods: 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. Results: 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. Conclusion: 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.
Databáze:	MEDLINE
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