Artigo
Human Platelet Antigen Genotype Is Associated With Progression of Fibrosis in Chronic Hepatitis C
Fecha
2012-01-01Registro en:
Journal of Medical Virology. Hoboken: Wiley-blackwell, v. 84, n. 1, p. 56-60, 2012.
0146-6615
10.1002/jmv.22191
WOS:000297456600009
6322604200510676
7805298466001457
3587895085226224
4619588334582084
7788448564326585
0000-0001-9200-5391
0000-0001-9200-5391
0000-0002-4035-9486
Autor
Universidade Estadual Paulista (Unesp)
Resumen
Although progression of fibrosis in the chronic hepatitis C depends on environmental, viral, and host factors, genetic polymorphisms have been associated recently with this progression, including the expression of integrins, adhesion proteins. Some integrins expressed on the platelet membrane show polymorphic antigenic determinants called human platelet antigens (HPA), where the major ones are HPA-1, -3, -5. The association between HCV infection and HPA-5b has been demonstrated. Similarly, the HPA profile could determine if HPA is related to progression of fibrosis. The goal of this study was to evaluate the association between the frequencies of HPA-1, -3, and -5 and degree of fibrosis in HCV-infected patients. Genomic DNA from 143 HCV-infected patients was used as the source for HPA genotyping by PCR-SSP or PCR-RFLP. Progression of fibrosis was evaluated using the METAVIR scoring system, and the patients were grouped according to degree of fibrosis into G1 (n = 81, with F1, portal fibrosis without septa or F2, few septa) and G2 (n = 62, with F3, numerous septa, or F4, cirrhosis). Statistical analysis was performed using the proportional odds model. The genotypic frequency of HPA-1a/1b was significantly higher in the patients in G2. To evaluate the influence of the time of infection to the development of fibrosis and its effect on the genetic factor HPA-1, 96 patients from 143 studied were evaluated considering the time of HCV infection, and these results suggest that the HPA-1a/1b genotype promotes the development of fibrosis in HCV infection with time. J. Med. Virol. 84: 56-60, 2012. (C) 2011 Wiley Periodicals, Inc.