{"id":{"repo_id":"auckland-ms","oai_identifier":"oai:researchspace.auckland.ac.nz:2292/53198"},"canonical_url":"https://search.dev.ndltd.org/etd/auckland-ms/oai:researchspace.auckland.ac.nz:2292/53198","repository":{"repo_id":"auckland-ms","name":"University of Auckland","base_url":"https://researchspace.auckland.ac.nz/server/oai/request"},"display":{"title":"Cell-Specific Inhibition of Interferon Production by Rotavirus","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.","abstract_html":"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.","abstract_has_math":false,"creators":["Shahrudin, Shabihah"],"institution":"ResearchSpace@Auckland","degree_name":"PhD","degree_level":"Doctoral","degree_discipline":"Biological Science","degree_department":null,"school":null,"contributors":[],"advisors":["Taylor, John"],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019","date_published":"2019","updated_at":"2026-07-24T01:04:34Z","subjects":[],"languages":[],"rights":["Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated."],"rights_urls":["https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm"],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/2292/53198","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Taylor, John"]},{"key":"dc:creator","label":"Author","values":["Shahrudin, Shabihah"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2020-10-08T02:20:35Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2020-10-08T02:20:35Z"]},{"key":"dc:date.issued","label":"Date","values":["2019"]},{"key":"dc:publisher","label":"Institution","values":["ResearchSpace@Auckland"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["UoA99265331310202091"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biological Science"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["PhD"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["The University of Auckland"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated."]},{"key":"dc:rights.uri","label":"Rights URI","values":["https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/2292/53198"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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."]},{"key":"dc:title","label":"Title","values":["Cell-Specific Inhibition of Interferon Production by Rotavirus"]}]}],"canonical_facts":{"dc:contributor.advisor":["Taylor, John"],"dc:creator":["Shahrudin, Shabihah"],"dc:date.accessioned":["2020-10-08T02:20:35Z"],"dc:date.available":["2020-10-08T02:20:35Z"],"dc:date.issued":["2019"],"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:identifier.uri":["https://hdl.handle.net/2292/53198"],"dc:publisher":["ResearchSpace@Auckland"],"dc:relation.isreferencedby":["UoA99265331310202091"],"dc:rights":["Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated."],"dc:rights.uri":["https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm"],"dc:title":["Cell-Specific Inhibition of Interferon Production by Rotavirus"],"dc:type":["Thesis"],"thesis:degree_discipline":["Biological Science"],"thesis:degree_level":["Doctoral"],"thesis:degree_name":["PhD"],"thesis:institution_name":["The University of Auckland"]},"updated_at":"2026-07-24T01:04:34Z"}