Date of Graduation
Winter 2024
Degree
Master of Science in Cell and Molecular Biology
Department
Biomedical Sciences
Committee Chair
Hulme Amy
Abstract
Human Immunodeficiency Virus 1 (HIV-1) is a lentivirus that infects CD4+ cells, causing a
weakened immune system that leads to the development of Acquired Immunodeficiency
Syndrome (AIDS). HIV utilizes host proteins to replicate. A genome wide screen by Brass has
shown that the molecular scaffolding protein, SPTBN1, is essential for HIV-1 infection.
However, the viral replication steps that SPTBN1 impacts are not known. Previous work in the
Hulme Lab has shown that SPTBN1 knockdown delays HIV capsid uncoating but does not
impact viral fusion kinetics. Uncoating and reverse transcription of HIV-1 occur simultaneously.
Therefore, the goal for this study was to analyze the impact of SPTBN1 on reverse transcription
of HIV-1 in microglial cells. Previous results indicating SPTBN1 as one of the host factors for
HIV-1 infection were confirmed in this research. SPTBN1 knockdown appeared to delay early
and intermediate reverse transcription, whereas late steps and completion of reverse
transcription did not seem to be affected. Future studies using the methods outlined in this
research would give insight into the host factors used in the infection process and could aid in
the development of future therapeutical targets for HIV-1.
Keywords
HIV-1, SPTBN1, reverse transcription, AIDS, microglial cells
Subject Categories
Medicine and Health Sciences
Copyright
© Jeanette Drecker
Recommended Citation
Drecker, Jeanette, "SPTBN1 Involvement in Reverse Transcription of HIV-1 Infection in CHME3 Cells" (2024). MSU Graduate Theses/Dissertations. 4031.
https://bearworks.missouristate.edu/theses/4031