David Robert McGivern, PhD

Assistant Professor of Medicine, School of Medicine


David McGivern Full SizeDivision of Infectious Diseases

Phone: (919) 843-4122
Email: david_mcgivern@med.unc.edu

CB# 7292, Burnett Womack Building
Chapel Hill, North Carolina 27599-7292





Education

PhD, University of East Angila, 2002

Research Interests

I am interested in the replication and pathogenesis of viruses that can infect the human liver, especially hepatitis C virus (HCV).

Chronic infection with HCV can lead to the development of fibrosis, cirrhosis, end-stage liver disease, and hepatocellular carcinoma (HCC). To understand the mechanisms that promote disease progression I aim to use multiple model systems, including in vitro systems and humanized mouse models, as well the study of tissue biopsy and serum samples from HCV-infected patients, to gain a more complete understanding of the interaction of HCV with the host. Within the HCV field, the careful quantitative experimental approaches that I employed in my research have helped resolve controversies such as the impact of HCV infection on the host cell cycle, DNA damage signaling pathways and apoptosis. I aim to combine basic and translational approaches to identify those factors, at the cellular and molecular level, that might be predictive of future disease outcomes (including HCC) during chronic HCV infection and in HIV/HCV co-infection. I expect this research to expand knowledge of the basic biology underlying pathogenesis in chronic HCV infection and ultimately, to better identify strategies to limit disease progression.

Novel direct-acting antivirals (DAAs) targeting the HCV life cycle have revolutionized treatment of chronic hepatitis C. New drugs recently approved by the FDA include inhibitors of the NS5A protein, a poorly characterized protein unique to hepaciviruses. My studies demonstrated that NS5A inhibitors can block virus assembly and release within a few hours and also suggested that NS5A inhibitors do not directly inhibit viral RNA synthesis but rather block assembly of the viral replicase complex. My future research in this area will focus on identifying the specific interactions of NS5A with host proteins that are blocked by NS5A inhibitors to gain a better understanding of the mode of action of this important class of drug.

Publications

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