Sebastian Winter - 2014 Merck-ICAAC Young Investigator Award Laureate

Winter Sebastian

Sebastian Winter, Ph.D., University of Texas Southwestern Medical Center, Dallas, has been honored with a 2014 Merck-ICAAC Young Investigator Award. Winter has received this honor for his outstanding work on bacterial pathogens, particularly Salmonella.

In 2006, Winter received his M. Sc. in Biochemistry from the University of Bayreuth. He then started his Ph.D. thesis research under the co-mentorship of Holger Rüssmann, University of Munich, and Andreas Bäumler, University of California, Davis, and studied mechanisms of innate immune evasion by Salmonella enterica serovar Typhi. In 2010, Winter obtained his Ph.D. in Human Biology from the University of Munich. His graduate work was recognized by the German Society for Hygiene and Microbiology with the BD Research Award in 2011. Winter continued his postdoctoral studies in Bäumler’s laboratory where he investigated alterations of the intestinal microbiota during episodes of inflammation. He discovered that the inflammatory host response changes the nutritional environment of the gut lumen by generating alternative electron acceptors as byproducts of the oxidative burst. Bäumler describes Winter as, “an impressive young scientist with a particular talent in developing innovative hypotheses and identifying the key experiments needed to tackle the corresponding gap in knowledge.”

In 2013, Winter joined the Microbiology Department at the University of Texas Southwestern Medical Center in Dallas and was named a member of the Endowed Scholars Program in Medical Science. His independent research group is investigating host-microbe and microbe-microbe interactions in the inflamed gut with a particular interest in infection with enteric pathogens and models of inflammatory bowel disease.

Presently, Torrent is a Marie Curie fellow at the Medical Research Council, Laboratory of Molecular Biology in Cambridge, England, where he is investigating the regulatory roles of tRNAs. These studies can help to understand, among other questions, how viruses manipulate tRNA populations to favor translation of their own proteins.



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