Presented By: Steeve Boulant, PhD
Speaker Biography: Throughout Steeve’s career, he has worked on multiple viruses (Hepatitis C virus, Reovirus, Hepatitis E virus, SARS-CoV-2, Astrovirus, Rotavirus). Steeve obtained his PhD from the University Lyon 1 in France where he worked on the structure of Hepatitis C virus capsid protein and discovered new open reading frames encoded by the virus. Following Steeve’s PhD, he went to Glasgow, Scotland where he continued his work on Hepatitis C virus but focusing on its life cycle. As a second postdoctoral experience, Steeve decided to change gears and went to Harvard Medical School where he studied the endocytic mechanisms of the enteric virus reovirus in human intestinal epithelial cells. In 2012, he established his own research group at the University Hospital Heidelberg, Germany where they focused on enteric viruse’s life cycle from receptor binding, entry into the host cell, replication and assembly, host antiviral response, and viral immune evasion….
Webinar: Impact of the Hypoxic Gut Microenvironment on Host Enteric Pathogen Interactions
Webinar Abstract: Intestinal epithelial cells lining the surface of our gastro-intestinal tract form a tight monolayer which serves as the primary barrier separating us from the luminal content of the gut. The lumen of the gut is home to a very complex commensal bacterial microbiota but also contains potential enteric viral (e.g. Rotavirus, Norovirus), bacterial (e.g Salmonella) and eukaryotic unicellular pathogens (e.g. Cryptosporidium). An important biochemical feature of our gastro-intestinal tract is the near absence of oxygen in the lumen of the gut known as the hypoxia environment. While it well established that hypoxia is critical to maintain a healthy microbiota, how the low oxygen environment impacts the response of intestinal epithelial cells to enteric pathogens remains unexplored. Here, we employed both intestinal cell lines and human intestinal organoids to monitor how hypoxia impacts the intrinsic immune response generated by intestinal epithelial cells upon enteric virus infection….
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