Bryce Duncan – Seminar/Ph.D. Defense, Monday, March 27, 2017 at 1:00 P.M.
JSNN – Bryce Duncan – Ph.D. Thesis Defense/Thursday Seminar
Candidate: Bryce Duncan
Advisor and Committee Chair: Christopher Kepley, Ph.D.
Date: Monday, March 27, 2017
Time: 1:00 P.M. – 3:00 P.M.
Location: JSNN Auditorium2907 E. Gate City Blvd., Greensboro, NC 27401
Title: “Studies Examining The Infectivity of Human Immunodeficiency Virus (HIV) on Human Mast Cells.”
Human immunodeficiency virus (HIV) establishes a latent infection in cells to ensure a persistent infection throughout an infected individual’s life. HIV can establish this latent infection in a variety of cells. Highly Active Anti-Retroviral Treatment (HAART) is a selection of drugs used to inhibit the production of new HIV and new infections and can effectively diminish virus population in blood. However, due to the pathological mechanism of the virus, it is not possible yet to completely eradicate virus as it remains immunologically invisible in latent cellular reservoirs. The cellular reservoirs where HIV evades the immune system are not known completely. Current research efforts are focused on identifying the cellular populations where HIV remains latent and determine how those latent reservoirs are established. By identifying latent cellular reservoirs where HIV resides strategies can be developed to target and kill infected cells or prevent emergence of virus. We hypothesized that primary skin-derived human mast cells may represent a previously unknown latent reservoir for HIV. Because mast cells can be activated through IgE-and non-IgE-dependent stimulation, we further hypothesized activated mast cells may be more vulnerable to infection. As described below our data suggest that skin-derived mast cells and their precursors are not susceptible to HIV infection even after activation through IgE and non-IgE-dependent pathways.
One strategy for inhibiting viral replication has been with fullerenes. Fullerenes are carbon spheres that can be functionalized for use in various biological systems. Fullerenes functionalized with large dendrimeric moieties have been shown previously to inhibit viral replication in vitro, but the majority of investigations that have explored fullerenes as an inhibitor of HIV were assessed computationally. Based on these previous studies we hypothesized that certain functionalized fullerenes will suppress HIV infectivity and/or replication. We hypothesized that these fullerenes may interact with HIV protease and performed molecular modeled docking studies to investigate this idea. As described below certain fullerene derivatives, depending on the moieties added to the carbon cage, were capable of inhibiting cellular infection. Thus, fullerenes may be a new way to inhibit HIV infection.