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Unlabelled: Information about HCV genotypes in infected patients from different regions of Mexico is limited., Objective: To determine the prevalence of HCV genotypes in a group of HCV infected patients who attended a third level Hospital in Northeast of Mexico., Methods: Genotyping analysis was performed using the InnoLiPA-HCV genotype assay in 147 patients (65 males and 82 females, mean age 44 +/- 12 years) with positive anti-HCV antibodies and detectable HCV-RNA levels., Results: Infected individuals were more likely to be female (56%). Histological data showed that 63% of the patients had chronic hepatitis, while the remainder presented cirrhosis (37%). The most frequent HCV genotype was 1 (73%). We found the following distribution: genotype 1 (2.7%), 1a (28.6%), 1b (37.4%), 1a/1b (4.1%), 2a (1.4%), 2b (8.8%), 2c (0.7%), 2a/2c (2.7%), 3 (2%), 3a (10.2%), 4 (0.7%) and 4c (0.7%). The most frequent associated risk factor was blood transfusion (72.5%)., Conclusion: Prevalence of HCV genotypes in the Northeast of Mexico is similar to those reported previously in other Mexican regions and the most frequent risk factor continues being blood transfusion.

The mechanisms by which alcohol exacerbates liver injury in patients with hepatitis C are unknown. We used the hepatitis C virus (HCV) subgenomic replicon cell system to evaluate the effect of ethanol on HCV replication and viral protein synthesis. Our results demonstrate that alcohol stimulates HCV replicon expression at both HCV-RNA and protein levels. Furthermore, we observed that ethanol treatment showed an additive effect in cyclooxygenase-2 (COX-2) protein expression and activity already induced by HCV viral proteins, and in turn increased HCV viral expression. Our results suggest that COX-2 activity is involved in ethanol-induced HCV-RNA and NS5A protein expression, because acetylsalicylic acid (ASA), a COX-1/2 inhibitor, blocked this induction and downregulated COX-2 protein expression and activity. Therefore, we suggest that ethanol increases HCV replication expression, at least in part, by upregulating a key cellular regulator of oxidative stress pathway known as COX-2 or its products.

Infection with hepatitis C virus (HCV) is a global public health issue. More than 200 million people in the world are infected with HCV. Hepatitis C is considered one of the main causes of chronic hepatitis, cirrhosis, hepatocellular carcinoma and liver transplantation. The identification of the viral genome quickly allowed delineation of genomic organization, and the structure and biochemical characterization of the proteins of HCV. However, it has been difficult to study its life cycle, as well as the development of antiviral agents due to the lack of a system of permissible culture. Numerous attempts have been reported to establish an in vitro system for the study of HCV. Recently, a system of efficient culture was established that allows replication of subgenomic molecules of HCV in a cell line of human hepatoma. In this revision, after a brief description of the molecular biology, means of transmission and clinical characteristics of hepatitis C, some of the experimental models are described that have been developed to date, focusing mainly on the subgenomic replicon system and their use in the development of new antiviral treatments.