dc.contributor.advisor |
Taylor, John |
en |
dc.contributor.author |
Shahrudin, Shabihah |
en |
dc.date.accessioned |
2020-10-08T02:20:35Z |
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dc.date.available |
2020-10-08T02:20:35Z |
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dc.date.issued |
2019 |
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dc.identifier.uri |
http://hdl.handle.net/2292/53198 |
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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. |
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dc.publisher |
ResearchSpace@Auckland |
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dc.relation.ispartof |
PhD Thesis - University of Auckland |
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dc.relation.isreferencedby |
UoA99265331310202091 |
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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 |
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dc.type |
Thesis |
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thesis.degree.discipline |
Biological Science |
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thesis.degree.grantor |
The University of Auckland |
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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 |
dc.identifier.wikidata |
Q112950237 |
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