*********************************
There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
*********************************
In partial fulfillment of the requirements for the degree of
Master of Science in Biology
in the
School of Biological Sciences
Qi An
Will defend her thesis
“THE EVOLUTIONARY BENEFITS OF LATENCY IN WITHIN-HOST HIV INFECTION DYNAMICS”
Wednesday, April 17, 2019
12:00 PM
Howie Physics N210
Thesis Advisor:
Dr. Joshua S. Weitz
School of Physics, School of Biological Sciences
Georgia Institute of Technology
Committee Members:
Dr. Samuel P. Brown
School of Biological Sciences
Georgia Institute of Technology
Dr. Daniel Coombs
Department of Mathematics
University of British Columbia
Abstract:
HIV is a retrovirus that infects helper T cells (CD4 + T cells) in the human immune system. At the cellular scale, HIV generates both actively and latently infected cells. Actively infected cells produce mature virions and are often the primary target of antiretroviral therapies. In contrast, latently infected T cells can do not produce virus particles, are hard to detect and treat, and can be reactivated to produce new virions. Understanding the dynamics of latent infections is critical to the development of strategies to treat and control the spread of HIV.
In this thesis, we study a variant of within-host models of HIV infection dynamics including proliferation of both susceptible and latently infected CD4+ cells. In this model, HIV infection of susceptible cells can result in acute or latent infections. The key innovation here is to identify the relative contributions of the active and latent pathways towards viral fitness, both in the initial and later stages of the within-host dynamics. We do so by leveraging a new approach to decomposing viral fitness developed in the context of phage- bacteria interactions. Our work highlights how variation in susceptible cell densities, viral life history traits, and retroviral therapies jointly influence dynamic selection pressures for active and latent infections.