Navegando por Palavras-chave "inibidor de protease"

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    Ação de cratabl, crataeva tapia bark lectin, em modelos experimentais de trombose arterial e diabetes induzidas em camundongos black 6 c57
    (Universidade Federal de São Paulo (UNIFESP), 2013-03-27) Salu, Bruno Ramos [UNIFESP]; Oliva, Maria Luiza Vilela Oliva [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    A hiperglicerina crônica nos quadros de diabetes é maior iniciadora de complicações microvasculares, como trombose arterial e é um importante alvo pra intervenções terapêuticas. Espécies de plantas do genêro.
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    Distribuição dos genótipos, caracterização de mutações que conferem resistência às drogas inibidoras de protease e os fatores de risco de transmissão do hcv em doadores de sangue de São Paulo
    (Universidade Federal de São Paulo (UNIFESP), 2015-05-02) Oshiro, Anna Shoko Nishiya [UNIFESP]; Sabino, Ester Cerdeira Sabino [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Nishiya, AS. HCV Genotypes, Characterization of Mutations Conferring Drug Resistance to Protease Inhibitors, and Risk Factors among Blood Donors in São Paulo, Brazil. São Paulo: Universidade Federal de São Paulo, Escola Paulista de Medicina. Background: Infection with Hepatitis C Virus (HCV) is a major cause of chronic hepatitis, affects 150 million people worldwide and is the cause of 350,000 deaths per year due cirrhosis or hepatocellular carcinoma. The aim of this study is to analyze the subtypes and existence of variants resistant to protease inhibitors and their association with potential HCV risk factors among blood donors in Brazil. Methods: Repeat anti-HCV reactive blood donors are systematically asked to return for retest, notification, and counseling in which they are interviewed for risk factors for transfusion-transmitted diseases. We analyzed 202 donors who returned for counseling from 2007 to 2010 and presented enzyme immunoassay- and immunoblot-reactive results. The HCV genotypes and resistance mutation analyses were determined by the direct sequencing of the NS5b and NS3 regions, respectively. The HCV viral load was determined using an in-house real-time PCR assay targeting the 5'-NCR. Results: HCV subtypes 1b, 1a, 3a and others genotypes (2b, 2c , 4 e 5) were found in 45.5%, 32.0%, 18.0% and 4.5% of the donors, respectively. The mean viral load of genotype 1 was significantly higher than that of genotype 3 isolates. Subtype 1a was more frequent among young donors and 3a among older donors. Protease inhibitor-resistant variants were detected in 12.8% of the sequenced samples belonging to genotype 1, and a higher frequency was observed among subtype 1a (20%) in comparison to 1b (8%). There was no difference in the prevalence of HCV risk factors among genotypes or drug-resistant variants. Conclusions: We found a predominance of subtype 1b, with an increase in the frequency of subtype 1a in young subjects. Mutations conferring resistance to NS3 inhibitors were frequent in treatment-naïve blood donors, particularly those infected with subtype 1a. These variants were detected in the major viral population of HCV quasispecies, have replicative capacities comparable to nonresistant strains, and could be important for predicting the response to antiviral triple therapy.