A.C. Cardoso 1 , C. Stern 1 , R. Moucari 1 , N. Giuily 1 , P. Bedossa 1 , P. Marcellin 1 1 Hopital Beaujon Background/Aim: This study evaluated the effect of the response (SVR) to therapy on fibrosis stage, as assessed by LS, in patients with advanced fibrosis (F3) or cirrhosis (F4). Methods: HCV patients with F3 or F4 who received interferon-based treatment were studded. LS was assessed after treatment (median delay of 36 months, 2-206) in patients with or without SVR. Correlations between LS and clinical and treatment characteristics were analyzed. Results: 114 patients were included: male gender (72%), mean age (54±9 years), diabetes (26%), mean BMI (26±6 kg/m2), genotype 1 (59%). 33% had SVR. LS was performed 0-3, 3-6, >6 years following treatment. By linear regression, the median of the LS was independently associated with SVR (p=0.005) and diabetes (P=0.008). SVR patients had lower LS (8.4 kPa; range 3.3-45) than non SVR patients (15.7 kPa; range 5.3-75) (p<0.001). Among the SVR patients the median LS was lower when the delay between LS and the end of treatment was longer (10.9,8.8,6. 3) (p=0.02). On the opposite, among the non-SVR patients the median LS was not significantly different (p=0.57). The median of liver stiffness was higher in patients with diabetes (p=0.006). BMI and dyslipidemia did not influence the median of the LS. Conclusion: In patients with advanced fibrosis or cirrhosis, LS was lower in patients with SVR and decreased with time while it was higher and did not decrease in non-SVR patients. LS could be important for assessment of fibrosis stage during the post-treatment follow-up. To study peripheral blood and intrahepatic Natural Killer (NK) cells in patients with chronic hepatitis C in relation to disease activity and severity of hepatic fibrosis. Patients & Methods: Fifteen untreated patients with histologically-proven chronic hepatitis C, and 12 matched healthy subjects. The NK cells and Natural Killer T (NKT) cells were identified in fresh whole blood samples using two-color flow cytometric assay as CD3 -CD56 + and CD3 + CD56 + positive cells. Immunohistochemical staining of liver biopsies taken from all patients was done using monoclonal antibody against CD56 for detection of NK cells and rabbit polyclonal antibody against smooth muscle actin (SMA) for identification of activated hepatic stellate cells (HSCs). Results: Patients with chronic hepatitis C showed significant decreases in the percentages of NK cells and NKT cells in peripheral blood. A negative correlation was found between serum HCV RNA levels and the percentages of peripheral blood NK cells and the intensity of intrahepatic NK cells. The percentages of circulating NK cells and NKT cells and the intensity of intrahepatic NK cells were inversely correlated with the METAVIR fibrosis stage and the steatosis grade, and also with the intensity of intrahepatic activated HSCs. Conclusion: Patients with chronic hepatitis C had significant deficiency in circulating NK and NKT cells as well as in intrahepatic NK cells. This may provide a possible mechanism for the suppression of innate immunity against HCV. Background: HCV infection is the major cause of chronic hepatitis, cirrhosis and hepatocellular carcinoma. The virus is classified in six genotypes and more 50 subtypes, which are related distinct with antiviral therapies reply. In Brazilian Amazon, epidemiologist's studies in blood donors had pointed high frequency of genotype 1 (74%) followed by genotypes 3 (25%) and 2 (1%). However, epidemiological research in populations of risk to the infection still is scarce. Aim: To determine HCV genotypic frequency in 116 blood donors, 55 patients with blood transfusions multiples, 57 patients in hemodialysis and 52 drugs users in the State of Pará, Brazilian Amazon. Methods: Using Real Time PCR and nucleotide sequencing followed phylogenetic analysis had been gotten viral diagnosis and genotyping. Results: In blood donors, HCV distribution was constituted by genotypes 1 (93.1%) and 3 (6.9%). In multitransfunded patients occurs maximum prevalence of genotype 1 (100%), probably reflect of genotype 1 specific transmission of blood donors population. On the other hand, in hemodialysis patients had been detected genotypes 1 (85.7%), 2 (3.6%) and 3 (10.7%), result of a bigger diversity of transmission routes (transfusional, interfamilial, nosocomial, etc) . In drug users occurs the biggest frequency of genotype 3 (38.1%) with prevalence of genotype 1 (61.9%), suggesting that the sharing of abuse machinery is allowing strains diffusion of genotype 3. Conclusions: The genotype 1 possesses the biggest frequency in different population. Moreover, through HCV genotypic frequency if it detached the contribution of transmission distinct routes indicated by previous epidemiologists researches. Virol. 2007 ). We established real-time polymerase chain reaction (PCR) assays for the easy detection of these HCV mutations. Methods: Plasmids p-core-W, including wild type HCV core coding region (70R and 91L), and p-core-M, including mutant type HCV core (70Q/H and 91M), were constructed by cloning and PCR-based mutagenesis for control vector of wild type core and that of mutant core, respectively. Using serially diluted forms of these vectors, SyBr Green-based real-time PCR detections with mutation-specific primers were performed. Results: Analysis of known scalar concentrations of references indicated that the detection limits of these methods were at least 10 copies, 10 copies, 1000 copies, and 10 copies of 70-wild, 70-mutant, 91-wild, and 91-mutant, respectively. Each primer could clearly distinguish the difference between p-core-W and p-core-M at the same copy numbers. Concerning substitution 70, the ratios 100:1, 10:1, 1:1, 1:10, and 1:100 of p-core-W versus p-core-M could be distinguished. On the other hand, for substitution 91, the ratios 100:1, 10:1, 1:1, 1:10, 1:100, and 1:1000 could be distinguished, confirming the sensitivity and specificity of the assay. Conclusions: This method could represent a useful alternative for the detection of genotype 1b HCV core amino acid substitutions 70 and 91 and be reliably applied for rapid screening.