title: Human platelet antigen genotype is associated with progression of fibrosis in chronic hepatitis C.
abstract: 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.
authors.affiliation: Gastroenterology Division, Department of Internal Medicine, Botucatu Medical School, Sao Paulo State University, UNESP, Botucatu-SP, Brazil.
authors.forename: Giovanni Faria
authors.initials: GF
authors.lastname: Silva
authors.forename: Rejane Maria Tommasini
authors.initials: RM
authors.lastname: Grotto
authors.forename: Camila Fernanda
authors.initials: CF
authors.lastname: Verdichio-Moraes
authors.forename: Silvia Maria
authors.initials: SM
authors.lastname: Corvino
authors.forename: Adriana Camargo
authors.initials: AC
authors.lastname: Ferrasi
authors.forename: Liciana Vaz de Arruda
authors.initials: LV
authors.lastname: Silveira
authors.forename: Maria Inês de Moura Campos
authors.initials: MI
authors.lastname: Pardini
mesh_terms: D000328:Adult; D016824:Antigens, Human Platelet / Q000235:genetics*; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000235:genetics*; D006801:Humans; D008103:Liver Cirrhosis / Q000235:genetics* / Q000473:pathology*; D008297:Male; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D018807:Polymorphism, Single-Stranded Conformational; D012720:Severity of Illness Index; D013997:Time Factors
chemical_list: D016824:Antigens, Human Platelet