Date of this Version
Zetterman, Allison. 2022. Using Zika Virus Plasmid to Increase Amyloid Precursor Protein in Alzheimer’s Disease Protein and Discovery of Novel IRF9 Protein. Undergraduate Honors Thesis. University of Nebraska-Lincoln.
Two projects are featured in this thesis, one focusing on increasing levels of amyloid precursor protein (APP) in Alzheimer’s disease (AD) proteins and the other outlining the discovery of a novel IRF9 protein. AD is a debilitating neurodegenerative disease characteristically featuring the development of amyloid-beta plaques and neurofibrillary tangles. The P2 plasmid from the Zika virus was converted into cDNA and injected into mouse models. Western blotting analysis was used to detect and analyze the presence and amplification of APP and tubulin. The addition of the P2 plasmid enhanced the levels of APP within the cell. This data will be helpful in further investigation into the mechanisms of AD and in designing a potential treatment for the disease. Interferon regulatory factors (IRFs) are transcription factors that activate Type I interferons. IRF9 is an important regulatory factor within the JAK-STAT signaling pathway, associated with cell immunity and other homeostatic processes. The Epstein-Barr virus has been known to persist in latency in B lymphocytes and regulate complex cellular regulatory networks. A novel protein, primate-specific (PS)-IRF9, was identified by the Zhang lab, and this experiment was done to confirm its presence. Cell lysates from Akata, IB4, and Jijoye EBV latency cell lines were used, and western blotting analysis was performed to analyze the presence of IRF9 variations. Akata is a Type I latency cell, whereas IB4 and Jijoye are Type II latency cells. The presence of PS-IRF9 was confirmed in the Akata cell lineage but absent in the IB4 and Jijoye cell lineage, showing a potential link between cell latency and different IRF9 proteins.