Liz Worthey

Liz Worthey, PhD, is faculty investigator and the director for software development and informatics at the HudsonAlpha Institute for Biotechnology in Huntsville, Alabama. Her work deals with clinical and translational use of genomic data.

Education

 * 1993, Undergraduate Fellow in Immunology, Stanford University, Palo Alto, CA
 * 1994, BS with Honors in Immunology, University of Glasgow, UK
 * 1994, Postgraduate Researcher in Molecular Biology, University of Glasgow, UK
 * 1994-1995, Graduate Researcher in Immunogenetics, Oxford University, UK
 * 1996, Postgraduate Diploma in Genetics, University of Birmingham, UK
 * 2003, PhD in Genetics, Imperial College, University of London, UK
 * 2000-2005, Postdoctoral Fellow in Genomics/Bioinformatics, SBRI/University of Washington, Seattle
 * 2005, Postdoctoral Fellow in Genomics, University of Washington, Seattle
 * 2005, Postdoctoral Training Course and Summer Research Program in Molecular Evolution, MBL, Woods Hole, MA
 * 2005, Postdoctoral Fellowship, A Practical Guide to Scientific Management for Postdocs and New Faculty, Howard Hughes Medical Institute/Wellcome Trust, HHMI headquarters, MD

Worthey's doctoral and post-doctoral researcher dealt with eukaryotic genomics and other high throughput “omics” projects.

Career
Worthey worked as a project manager for Merck & Co., then in 2008 joined the Medical College of Wisconsin (MCW) as senior research scientist. She became an assistant professor of pediatric genomics in 2010, then director of genomic informatics at the MCW Human and Molecular Genetics Center in 2012. She is also an adjunct assistant professor in the computer science department at the University of Wisconsin – Milwaukee and adjunct assistant professor in the department of pediatrics and department of genetics at the University of Alabama at Birmingham.

She joined HudsonAlpha Institute for Biotechnology in 2015.

ME/CFS research
In 2018, Worthey received a Ramsey Award program grant to pursue a whole genome sequencing project on ME/CFS that hypothesizes the disease "is the result of an intrinsic genetic defect(s) that alters cellular metabolic homeostasis towards an unstable state."