Date of Graduation
Spring 2022
Degree
Master of Science in Cell and Molecular Biology
Department
Biomedical Sciences
Committee Chair
Amy Hulme
Abstract
HIV-1 is the etiological agent that cause AIDS. Since the 1980’s when HIV-1 was discovered, much has been discovered, however a cure for HIV-1 has eluded researchers. Effective therapeutics do exist but can have adverse side effects including HAND/HAD which leads to neurodegeneration in patients regardless of viral suppression. One area of research that holds the possibility of discovering new viral targets and therapeutics is host factor interaction within the replication process. One host factor that can cause a decrease in HIV-1 infectivity is SPTBN1. SPTBN1 is a cytoskeletal protein that was shown to bind to the capsid and nucleocapsid proteins of HIV. However, the exact mechanism of SPTBN1 involvement in HIV-1 infection is still unknown. Here we utilized siRNA to downregulate SPTBN1expression and ascertain the role it plays in HIV-1 infection. When SPTBN1 was downregulated, there was a 19.75% decrease in the infectivity of HIV-1. A mini-CsA washout assay was then performed to assay capsid uncoating at the early time points. At the 30 min time point there was a 9% decrease in uncoating and a decrease of 24% at 1hr when SPTBN1 expression was downregulated. From these results, the decrease in infectivity could be caused by the decrease in uncoating. However, it is still unknown if SPTBN1 plays a part in the other replication steps of HIV-1 and more research is needed to divulge the full role SPTBN1 plays in HIV-1 infection.
Keywords
HIV-1, microglial cells, uncoating, SPTBN1, HAD/HAND, infectivity
Subject Categories
Immunology and Infectious Disease | Life Sciences | Virus Diseases
Copyright
© Marc Gordon Havlicek
Recommended Citation
Havlicek, Marc Gordon, "The Role of the Host Factor SPTBN1 in HIV-1 Infection of Microglial Cells" (2022). MSU Graduate Theses. 3709.
https://bearworks.missouristate.edu/theses/3709
