Day 2 :
Temple University, USA
Keynote: Symbiotic bacteria provide chemoprevention against hepatitis B virus mediated hepatocellular carcinoma in hepatitis B x transgenic mice
Time : TBD
Mark A Feitelson received his PhD in Microbiology and Immunology in 1979 from the UCLA School of Medicine. He was an American Cancer Society Post-doctoral Fellow at Stanford University from 1980-82, and was then recruited to the Fox Chase Cancer Center by Dr. Baruch Blumberg (Nobel laureate). In 1991, he became Associate Professor of Pathology and Cell Biology and Head of the Molecular Diagnostics Lab in Microbiology at Thomas Jefferson University. In 2007, he moved to Temple University, where he is now Professor of Biology. His research on hepatitis B and liver cancer has been supported by NIH for more than 25 years, has more than 130 publications, and is presently Head of the Professional Science Master’s program in Biotechnology at Temple University.
Chronic infection with hepatitis B virus (HBV) is associated with the development of progression of chronic liver disease (CLD) and the appearance of hepatocellular carcinoma (HCC). HCC is a prevalent cancer worldwide with few treatment options. Given that HCC develops most often on the background of chronic inflammation, experiments were designed to test the hypothesis that selected probiotic bacteria that suppress inflammation could be used as a simple and inexpensive means to prevent or delay the appearance of HCC. To test this, hepatitis B x (HBx) transgenic mice, which develop progressive liver lesions that culminate in HCC, were treated with a mixture of probiotic bacteria (Synbiotic 2000). The result showed a significant reduction in the number and size of dysplastic and HCC nodules compared to control transgenic mice. Microarray analysis of selected immune and cancer associated markers showed a strong reduced expression in the liver of mice treated with Synbiotic 2000 compared to controls. Thus, Synbiotic 2000 attenuates the pathogenesis of HCC, and may be useful in cancer chemoprevention, not only for HCC, but perhaps against other cancers that often develop on the background of chronic inflammation.
Cancer Research Center of Lyon, France
Time : TBD
Eve-Isabelle Pecheur has completed her PhD in 1997 from University Paris XI and Post-doctoral studies from Groningen University of Medical Sciences (Netherlands). She leads a research group at the Cancer Research Center of Lyon. She has published more than 50 papers in reputed journals. She is serving as an Editorial Board Member of Antiviral Research, and as an Academic Editor of PLoS ONE.
Viruses are obligate intracellular agents that depend on host cells for successful propagation, hijacking cellular machineries to their own profit. The hepatitis C virus (HCV) is a strictly human pathogen, causing chronic liver injuries accompanied by lipid disorders. Upon infection, in addition to protein-protein and protein-RNA interactions usual for such a positive-strand RNA virus, HCV relies on protein-sugar and protein-lipid interactions at multiple steps of its life cycle to establish persistent infection. En route from the blood stream to hepatocytes of the liver, its target cells, HCV encounters a specific micro-environment at the surface of hepatocytes, comprising glycoproteins, proteoglycans and polysaccharides, called the glycocalyx. Protein-sugar interactions therefore occur, that I will explore to address how HCV infection modulates the hepatocyte glycocalyx, and in return how this peculiar region of the cell adapts to the persistent presence of the virus. After this journey through the glycocalyx, HCV penetrates into the hepatocyte, which relies on subtle protein-protein and protein-lipid interactions dissected through structural, biochemical and biophysical analyses. HCV infection subsequently leads to a major reshuffle of the endoplasmic reticulum, the intracellular compartment where viral replication takes place, implying intense underlying protein-lipid interactions. I will also explore how de novo production and assembly of viral particles are inseparable from cellular lipid metabolism, since lipoproteins are structural components of neoformed virions. Each of these steps are potential therapeutic targets, which will be discussed at the light of current antiviral strategies.