Katherine Valente
Pronouns: she/her
Research Mentor(s): Tomoyuki Murakami
Research Mentor School/College/Department: Microbiology & Immunology / Medicine
Program:
Authors: Katherine Valente , Kai-Neng Chou, Tomoyuki Murakami
Session: Session 2: 10:00 am – 10:50 am
Poster: 88
Abstract
Human Immunodeficiency Virus (HIV) is a virus that attacks the human immune system. The virus specifically infects CD4+ T-cells, which impacts the body’s ability to effectively fight against diseases and other viruses. HIV establishes a latent infection. Latent viral reservoirs reside within infected individuals around secondary lymphoid organs (SLOs). These viral reservoirs are barriers for a cure for HIV because they cannot be eliminated by Antiretroviral Therapies (ART) and have the ability to eventually reactivate upon ART interruption. Lymph nodes, one of SLOs, contain fibroblastic reticular cells (FRCs) that organize lymph node structure and facilitate T-cell movement throughout the body. Previously, our group discovered that FRCs accelerate HIV-1 proliferation through direct interactions with both HIV-1 and T-cells. In addition, our preliminary results suggest that FRCs enhance HIV-1 spread via the secretion of Galectin family proteins without direct interactions with at least HIV-1. However, which Galectin proteins contribute to this enhancement is unknown. Since previous literature suggests that the presence of Galectin-9 supports higher rates of T-cell infection by HIV-1, we sought to determine whether Galectin-9 expressed by FRCs facilitates HIV-1 infection of T-cells. We constructed a Galectin-9 expression plasmid with the mRNA isolated from FRCs. Galectin-9 expression in HeLa cells transfected with the plasmid was determined by Western Blotting. T-cells will be co-cultured with HeLa cells transfected with the plasmid and infected with HIV-1. Infection efficiency will be measured to determine the effect of Galectin-9 on virus infection among T-cells. In future studies, whether FRC-derived Galectin-9 promotes HIV-1 production from viral reservoirs will be tested. Targeting a singular protein that can potentially be a factor for HIV proliferation throughout the body would be very promising for the future of HIV treatment.
