Hepatitis C virus (HCV) infection is the major cause of chronic hepatitis worldwide, with an overall prevalence of approximately 3% with more than 170 million individuals infected. The results of treatment protocols based on the association of Pegylated interferon-± (IFN±-PEG) with Ribavirin (RBV) are unsatisfactory, only 50% of the infected individuals with HCV genotype 1 achieve sustained virological response (SVR). Thus, it is necessary to explore new therapeutic approaches targeting both viral and host factors, in order to modulate the immunity and control viral infection. It has been reported that a microRNA (miRNA) expressed specifically in the liver (miR-122) has the ability to bind at two sites in the 5' UTR of HCV genome acting as a positive regulator of replication. This miRNA also has been implicated as a regulator of lipid metabolism, but the mechanism involved in this regulation is still unclear. Recent studies showed that a LNA (Locked Nucleic Acid) molecule complementary to miR-122 not only dramatically inhibited viral replication but also altered the expression of genes involved in lipid metabolism, for example, decreasing the expression of miR-33a. The miR-33a is a key regulator in lipid metabolism as its inhibition may result in increased fatty acid oxidation and accumulation of fat in the liver. In the current study, we will evaluate miR-33a and miR-122 expressions on liver tissue from patients infected with HCV genotypes 1 and 3. The comparative analysis of expression data will allow the evaluation in the profile of these molecules in infections caused by the most frequent HCV genotypes in Brazil.
News published in Agência FAPESP Newsletter about the scholarship: