Computational systems biology analysis of changes in gene regulation during Flaviviridae virus infection
Abstract
Flaviviridae viruses cause thousands of deaths and threaten millions of people in the world each year. Despite widespread studies, the underlying host-virus functional interactions in the Flaviviridae virus infected host cells are poorly understood. Using computational systems biology methods, this study focuses on analyzing the high-throughput expression data including DENV, WNV, HCV and HIV. HIV does not belong to the Flaviviridae family, and is used as a comparison. Using a meta-analysis approach, differentially expressed genes in host cells have been identified. Significant Gene Ontology terms and enriched pathways have been determined based on result of the meta-analysis. Comparing the enriched pathways across different Flaviviridae viruses, two pathways have been revealed to be in common in all three Flaviviridae viruses: hsa04060 (Cytokine-cytokine Receptor Interaction) and hsa04062 (Chemokine Signaling Pathway). Interestingly, hsa04060 was also enriched during HIV infection, thus making it non-specific to Flaviviridae viruses. The study provided with what genes were differentially expressed, and what GO terms and pathways were enriched, showing the meta-analysis as a good tool for elucidating the host-virus functional interaction during Flaviviridae virus infection.
Degree
M.S.
Advisors
Gribskov, Purdue University.
Subject Area
Systematic|Bioinformatics
Off-Campus Purdue Users:
To access this dissertation, please log in to our
proxy server.