Date of Graduation

Fall 2022

Degree

Master of Science in Cell and Molecular Biology

Department

Biomedical Sciences

Committee Chair

Amy Hulme

Abstract

Human immunodeficiency virus (HIV) is a chronic illness affecting more than 32.7 million individuals worldwide. The virus infects immune cells, weakening the immune system overtime eventually leading to acquired immunodeficiency syndrome (AIDS) if left untreated. Infection starts with a fusion step, followed by uncoating of the HIV capsid once in the cytoplasm of the cell. HIV uses host cell proteins to complete the infection process, like the actin associated factor, SPTBN1. The Hulme lab has previously shown that SPTBN1 knockdown by siRNA in microglial cells decreased HIV infection and delayed uncoating of HIV. Because fusion is prior to uncoating, it is important to verify that fusion delay was not the reason uncoating was delayed. The goal of this thesis research was to further determine the role of SPTBN1 in HIV infection of microglial cells that are a natural host for HIV. The siRNA knockdown of SPTBN1 was optimized, achieving knockdown between 67-94%. A knockdown of SPTBN1 was done to confirm that it decreases infection, and the fusion kinetics were observed by a fusion assay. The fusion step of HIV infection was determined to not be affected by SPTBN1 knockdown with fusion kinetics being similar to control conditions. These results support the labs previous conclusion that SPTBN1 is involved in the uncoating step of HIV infection that follows fusion. Researching hosts factors such as SPTBN1 provide important insights to how HIV infects cells and identifies areas of interest that can be targeted by medications.

Keywords

HIV-1, microglial, SPTBN1, cytoskeleton, actin

Subject Categories

Medical Sciences | Nervous System Diseases | Other Public Health | Virus Diseases

Copyright

© Hannah Matheney

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