Abstract

Vesicular stomatitis virus (VSV) is a negative sense, single-stranded RNA (ssRNA) virus that is currently studied for its uses as a vaccine viral vector and its potential in oncolytic therapy. The M protein of VSV is the active participant in the virus’s abrogation of the host innate immune response. This activity is thought to be due to the M protein’s ability to downregulate overall host transcription by blocking nuclear transport. A VSV mutant containing a D52G mutation in the M protein (22-20) has been shown to block nuclear transport while being defective as a suppressor of NF-κB activation. It is thus believed that while previous M protein mutant viruses are defective in both host transcription suppression and NF-κB activation, 22-20 is deficient in only one of these activities. This study aims to identify differentially expressed genes (DEGs) and pathways through transcriptome analysis of host response to VSV mutants. Our research leads us to believe that 22-20 does in fact down regulate overall host transcription, while being inefficient in suppressing NF-κB mediated immune response pathways. We also discovered important DEGs in the apoptosis pathway, including the antiapoptotic protein Mcl1, where downregulated by 22-20 to a greater degree than another mutant, 22-25. This combination of factors, deficiency in NF-κB suppression and increased apoptotic activation, could make 22-20 an interesting candidate for oncolytic research.

Publication Date

12-14-2018

Document Type

Thesis

Student Type

Graduate

Degree Name

Bioinformatics (MS)

Department, Program, or Center

Thomas H. Gosnell School of Life Sciences (COS)

Advisor

Maureen C. Ferran

Advisor/Committee Member

Feng Cui

Advisor/Committee Member

Matthew Morris

Campus

RIT – Main Campus

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