Date of Graduation

Spring 2025

Degree

Master of Science in Biomedical Sciences

Department

School of Heath Sciences

Committee Chair

Amy Hulme

Abstract

Human immunodeficiency virus (HIV) directly attacks the host immune system by infecting and replicating in CD4-presenting immune cells. Like most viral pathogens, HIV utilizes cellular machinery to assist in viral entry, transport, and export. One of the components HIV is known to utilize for replication is the actin cytoskeleton. By directly binding to actin or actin-binding proteins, HIV can manipulate structural dynamics within the cell. The way HIV hijacks actin for replication post-viral fusion isn’t fully understood, especially during viral transport to the nucleus. A 2013 study conducted by Dai et al. found that lowering the expression of the cellular protein spectrin β non-erythrocyte 1 (SPTBN1) in macrophages led to HIV-resistant cells and partial depolymerization of the actin cytoskeleton. This thesis investigates the role of SPTBN1 in the early stages of HIV replication and localization within CHME3 microglial cells. Through fluorescent microscopy, SPTBN1 and overall actin structure in CHME3 cells were visualized. The results indicated colocalization between SPTBN1 and actin, with 90% of SPTBN1 overlapping with actin. Additionally, SPTBN1 knockdown did not cause consistent observable changes in the actin cytoskeleton. Colocalization between SPTBN1 and HIV was also observed. Future research will use these techniques to determine how SPTBN1 knockdown affects HIV-1 colocalization in CHME3 cells. Overall, these findings contribute to a better understanding of the role host cell proteins play in HIV replication.

Keywords

HIV-1, SPTBN1, actin, colocalization analysis, microglia, fluorescence microscopy

Subject Categories

Medicine and Health Sciences | Virus Diseases

Copyright

© Rachel Pecka

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