Cell-Specific Inhibition of Interferon Production by Rotavirus

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dc.contributor.advisor Taylor, John en
dc.contributor.author Shahrudin, Shabihah en
dc.date.accessioned 2020-10-08T02:20:35Z
dc.date.available 2020-10-08T02:20:35Z
dc.date.issued 2019
dc.identifier.uri http://hdl.handle.net/2292/53198
dc.description.abstract Rotavirus (RV) is a leading cause of diarrhoea in young children. In 2016, rotavirus-related death was estimated around 128,500, with 258,173,300 episodes of diarrhoea in children below 5 years. Although extra-intestinal rotavirus infection is limited, the spread of the virus can cause seizures and pancreatitis. Rotavirus non-structural protein 1 (NSP1) is responsible for viral evasion of the innate immune system, the first line of defence against invading pathogens. The activated immune system produces interferon (IFNs), a cytokine that drives expression of antiviral effectors, known as IFN-stimulated genes (ISGs). The studies reported in this thesis investigate the differences in rotaviral infection of two human cell lines; the intestinal (Caco-2) and the alveolar basal (A549) epithelial cells. Our findings confirmed the potential ability of the virus to establish extra-intestinal infection in A549 cells. Furthermore, our results showed up-regulated IFNs and ISGs transcription in RV-infected A549 cells, which was absent in infected Caco-2 cells. While NSP1 was known to mediate degradation of IRF3 to antagonise the host immune response, the differences observed between Caco-2 and A549 cells were not due to IRF3 degradation. This study highlights the distinct transcriptional profile following virus replication; Caco-2 cells infected with replication-deficient RV induced transcription of IFNs and ISGs to a similar extent as infected A549 cells. However, this response was abrogated only in Caco-2 cells in the presence of replication-competent RV, suggesting differences in virus-host interactions that allowed A549 cells to produce IFNs.
dc.publisher ResearchSpace@Auckland en
dc.relation.ispartof PhD Thesis - University of Auckland en
dc.relation.isreferencedby UoA99265331310202091 en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/nz/ en
dc.title Cell-Specific Inhibition of Interferon Production by Rotavirus en
dc.type Thesis en
thesis.degree.discipline Biological Science
thesis.degree.grantor The University of Auckland en
thesis.degree.level Doctoral en
thesis.degree.name PhD en
dc.date.updated 2020-09-16T07:52:34Z en
dc.rights.holder Copyright: The author en
dc.rights.accessrights http://purl.org/eprint/accessRights/OpenAccess en

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