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CSE Seminar - Roy Dar / Genetic coupling of viral-host gene expression presents migratory challenges in HIV therapies

Event Type
Computational Science and Engineering
NCSA Room 1030
Apr 20, 2017   12:00 - 1:00 pm  
Dr. Roy Dar
Originating Calendar
Computational Science and Engineering (CSE) Seminars


Roy Dar is an Assistant Professor in the Department of Bioengineering and affiliate at the Carl R. Woese Institute for Genomic Biology, and the Center for Biophysics and Quantitative Biology at the University of Illinois at Urbana-Champaign. He received his B.Sc. in Physics and Mathematics from the Hebrew University of Jerusalem, Israel in 2004 and his Ph.D. in Physics (Biophysics and Systems Biology) from the University of Tennessee, Knoxville and Oak Ridge National Laboratory in 2011. Prior to joining UIUC in 2015, Roy pursued his postdoctoral research at the Gladstone Institutes for Virology and Immunology at the University of California, San Francisco where he studied the fundamentals and exogenous drug control of stochastic fluctuations to affect stability of HIV-1 latency and decision-making in single cells. Roy’s research focuses on the fundamentals and application of modulating gene expression noise in individual cells for a functional advantage as well as systems biology, cellular organization principles, and viral-host interactions.


Viral-host interactomes map the complex architecture of an evolved arms race during host-cell invasion. mRNA and protein interactomes have revealed elaborate targeting schemes, yet evidence for genetic coupling, resulting in the co-regulation of promoters, remains elusive. I will present a genetic to single-cell study from our lab using computational and experimental approaches on viral-host interactomes of human immunodeficiency virus (HIV), and its ability to genetically couple and co-regulate itself with endogenous pathways throughout the human genome. We find that viral-host co-evolution is imprinted within promoter gene sequence, i.e. prior to transcript or protein interactions. Discovered co-regulation of HIV and a major chemokine receptor facilitates migration of infected cells. Upon infection, HIV can either actively replicate or remain dormant. Cells producing virus pose a risk for reinitiating infection within niches inaccessible to drug treatments, and tuning viral control of migration and reactivation improves strategies to eliminate latent HIV. Viral-host genetic coupling establishes a novel mechanism for synchronizing transcription and guiding potential therapies.

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