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Examining the role of the host helicase DDX56 during Flavivirus infections Open Access


Other title
Viral-host interactions
RNA Helicases
Type of item
Degree grantor
University of Alberta
Author or creator
Reid, Colleen R.
Supervisor and department
Hobman, Tom C. (Cell Biology)
Examining committee member and department
Evans, David (Medical Microbiology and Immunology)
Marchant, Davd (Medical Microbiology and Immunology)
Montpetit, Benjamen (Cell Biology)
Department of Medical Microbiology and Immunology
Date accepted
Graduation date
Master of Science
Degree level
Flaviviruses, such as West Nile virus (WNV), Powassan virus (POW), and Saint Louis encephalitis virus (SLEV), are significant pathogens capable of causing serious neurological disease in both humans and animals. Despite their relevance to human health, treatment and vaccines for these viruses remain limited. Characterizing important cellular host factors during viral infection may identify novel targets for the development of antivirals. Previously, a host nucleolar RNA helicase, DDX56, was identified as an essential host factor for WNV infectivity by utilizing its ATP-dependent helical activity to enhance the packaging of viral RNA. Through extensive microscopy analyses I show that DDX56 localizes to the ER, the site of viral replication and assembly, during WNV infection and colocalizes with markers for viral assembly. Additionally, DDX56 does not play a role in the reorganization of membranes and the induction of viral structural elements in WNV infection. Together, these data support the role of DDX56 in assembly of infectious virions. I also investigated whether other viruses, POW and SLEV, utilize DDX56 during infection making it a potential target for broad-spectrum antivirals. Interestingly, while I discovered that these viruses affect DDX56 localization and stability, they do not require this helicase for the production of infectious virions. Thus, DDX56 seems to be an essential host factor for WNV while the underlying mechanism of relocalization may not be virus specific. Collectively, my studies further our understanding of the role of DDX56 during WNV infection and further support it as a target for the development of antivirals.
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