6^th World Congress on Hepatitis & Liver Diseases June 18-20, 2018 Dublin, Ireland

Dr. Mark Feitelson received his Bachelors of Science (BS) degree in biology/biochemistry from UCI in 1974. He was a graduate student in the Department of Microbiology and Immunology at the UCLA School of Medicine, where he began is studies of viral oncogenesis with the rabbit papilloma virus, and received a Ph.D. degree in 1979. He was then an American Cancer Society Postdoctoral Fellow in the Department of Medicine at Stanford University, where he began his work with hepatitis B and related viruses. Dr. Feitelson was then recruited to the Fox Chase Cancer Center in Philadelphia, where he trained with Dr. Baruch Blumberg, who won the Nobel Prize in medicine (1976) for his discovery of HBV. When Dr. Blumberg went to Oxford (1990), Dr. Feitelson became an Associate Professor in Department of Pathology, Anatomy and Cell Biology at Thomas Jefferson University (1991), and later Full Professor (1996). At Jefferson, he was a member of the Kimmel Cancer Center, and Director of the Molecular Microbiology Lab at the university hospital. In 2007, Dr. Feitelson moved to the Department of Biology at Temple University. His lab has produced more than 130 publications, which include two books, many book chapters, and numerous invited reviews. Dr. Feitelson belongs to several scientific societies and was a visiting professor at five universities in China. His lab has been funded by NIH, pharmaceutical firms, and by foundations for more than 30 years. Since the early 1980's, Dr. Feitelson has been interested in the pathogenesis of chronic hepatitis B virus infection and has uncovered critical steps whereby the HBV encoded X antigen contributes to the pathogenesis of chronic liver disease and the development of HCC. He has also developed a program studying the relationship between the gut microbiome and various disease states and has recently founded a company based on a platform technology. Finally, Dr. Feitelson is the head of the Professional Science Master's Program in Biotechnology at Temple, which has been highly successful over the past few years.

Pathogenesis of chronic hepatitis B virus infection

Michel Samson has got his PhD in 1993 at University of Paris XI (France). He studied as postdoctoral scientist at Université Libre de Bruxelles (Brussels, Belgium) supported by prestigious fellowships (EMBO, European Community, etc..). He passed two years as visiting scientist at Genentech (California, USA). He is now team leader and director of research of Inserm at University of Rennes (France) in UMR 1085 Inserm, vice-director of Institut de Recherche en Santé, Environnement et Travail. He studies the inflammation, cell death and fibrosis in liver pathologies. He has published more than 90 papers in reputed journals (Nature, Cell, J Exp Med, Hepatology, J Hepatol., etc...), with already more than 8400 citations and H-index 37.

Liver pathologies due to infectious agents including mainly hepatitis B and C viruses, use of some drugs or metabolic syndrome constitute real public health problems. During liver injury, cytokines play a central role in the orientation of the immune response to an effective response or not and in the establishment and maintenance of the inflammatory response, which when it becomes chronic is at the origin of dysfunctions of the liver. Our team's work focuses on studying the role of new cytokines or immunomodulatory factors (chemokines, IL-33, soluble HLA-G, etc.) and of their associated receptors in liver pathologies. We are also interested in the type of death of hepatocytes induce by cytokines such as TNF, FASL or TRAIL. We recently showed, by the use of RIPK1 kinase dead mice (Ripk1K45A) or a RIPK1 kinase activity inhibitor (Nec-1s) that blockade of RIPK1 kinase activity reduced hepatolysis during immuno-dependent hepatitis. Furthermore, using conditionally deficient mice for RIPK1 in hepatic parenchymal cells (Ripk1LPC-KO), we observed an increase in the susceptibility of mice to ConA-induced hepatitis or to the administration of PAMPs (LPS or CpG-unmethylated DNA). We have demonstrated that this hepatocyte death is apoptotic and is dependent on TNF-α produced mainly by activated macrophages. FasL alone or the IFNγ plus TRAIL combination also sensitizes the hepatocytes of Ripk1LPC-KO mice to apoptotic death. This project is currently underway to show the role of RIPK1 in infectious hepatitis, in nonalcoholic steatohepatitis (NASH) or in drug-induced liver injury.

Dr. med. Hani Oweira, is a visceral Surgeon working in the Hirslanden Hospital Group in Zurich and Cham in Switzerland. He was trained in Charite Berlin and the University Hospital in Heidelberg in Germany. His Research focused on the predictive markers for liver dysfunction after liver surgery and transplantation.

Total pancreatic surgery, Hepatic surgery, Surgery for hepatic metastases, Minimally invasive surgery, Endocrine bowel surgery and Hernia surgery.

João R. Mesquita (D.V.M., M.Sc.; Ph.D.) is a Professor at the Polytechnic Institute of Viseu where he teaches topics within Infectious Diseases for more than 10 years. On the past decade he has focused on Virology, where he has published 44 papers in Scopus indexed Journals. He has won several scientific prizes from different societies and conferences, where he has presented numerous oral and poster presentations.

His research interests are focused on animal and human virology, mainly on zoonotic viruses, with special interest on surveillance tools and epidemiology.