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Ann L. Wozniak, Ph.D.

Ann Wozniak portrait
Assistant Professor, Gastroenterology, Hepatology & Motility

Professional Background

Dr. Wozniak is an Assistant Professor and member of the Liver Center at the University of Kansas Medical Center.

Dr. Wozniak received her BS from the University of Wisconsin-Madison where she studied aspects of mammary tumor cell biology. Dr. Wozniak then obtained her PhD from the University of Texas Medical Branch where she examined the role of the Hepatitis C Virus p7 ion channel in the viral lifecycle, and demonstrated that p7 prevents the acidification of virus-containing vesicles, preserving the infectivity of secreted virions. Her post-doctoral work at the University of Kansas-Medical Center investigated viral effects on cellular trafficking with a goal of understanding how HCV reroutes a number of cellular trafficking events such as autophagy, lysosome-endosome fusion and secretion to promote its lifecycle.

Dr. Wozniak's current work is at the intersection of basic cell biology and liver disease and examines inflammation-induced modification of Rab adaptor proteins. her team investigates how inflammation alters the intracellular trafficking of vesicles, secretion of exosomes, and the selection of key exosome cargo. The ultimate goal of Dr. Wozniak's research is to improve clinical outcomes for patients with inflammatory liver disease.

Education and Training
  • BS, Biology, University of Wisconsin-Madison, Madison, WI
  • PhD, Cell Biology, University of Texas Medical Branch, Galveston, TX
  • Post Doctoral Fellowship, Pathogenesis of Hepatitis C Virus, University of Kansas-Medical Center, Kansas City, KS
Professional Affiliations
  • American Society of Cell Biology, American Society of Cell Biology, Member, 2022 - Present
  • Society of Toxicology, Member, 2021 - Present
  • AASLD (American Association for the Study of Liver Diseases), Member, 2017 - Present



Inflammation, cellular trafficking, and exosome biogenesis: Inflammatory stimuli and diseases produce a burst of exosome production from affected cells. These exosomes play an important role in cell-cell communication and modulate host responses. These "inflammatory exosomes" have distinct protein and RNA content and are different in both quantity and composition from exosomes produced from the same cells prior to inflammation. Our lab discovered that caspase-1 cleaves a Rab7 adaptor protein called RILP. This cleavage repositions cellular vesicles and leads to an enhancement of plasma membrane fusion events which accounts for the burst of exosome secretion observed during cellular inflammation. Current studies are investigating the molecular details of these interactions, how they determine exosome cargo specificity, and how they can be manipulated to improve the outcome of inflammatory liver disease.

SARS-CoV-2 and host cell interactions: Another ongoing project in the lab investigates the mechanisms by which SARS-CoV-2 modulates cellular trafficking. SARS-CoV-2 is unusual among human viruses for the very high level at which it is shed and the occurrence of super-spreader events which result from a combination of human behavior and unusually high viral shedding. However, the reasons why the virus is able to undergo these rapid transmission events is not understood. Our lab had previously examined the factors that are responsible for efficient shedding of the hepatitis C virus (HCV). We discovered that HCV uses a viral protein called a viroporin to activate a series of events that ultimately causes the cleavage of a cellular protein, RILP, that controls the movement of vesicles within the cell. RILP cleavage severs the linkages that hold newly formed virus particles in the cell and essentially causes them to shoot out of the cell into the environment. Our lab is currently investigating the mechanisms of cellular trafficking modulation by SARS-CoV-2 and examining how manipulating the RILP trafficking axis affects SARS-CoV-2 viral shedding and inflammatory response.

Neuroinflammation and Endocytic Trafficking in Alzheimer’s Disease: Chronic inflammation is a ubiquitous feature of Alzheimer’s disease and has been proposed to exacerbate the formation of both amyloid plaques and NFTs (neurofibrillary tangles). Another project in our lab investigates how Alzheimer’s disease-induced neuroinflammation alters the endocytic pathway to enhance and promote disease progression. The work lends insight into new druggable targets for Alzheimer disease.