https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7293 Sat 24 Mar 2018 08:42:13 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7208 Sat 24 Mar 2018 08:39:57 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26099 TM Western assays. Transepithelial permeability assays were performed to assess effects on barrier functionality. RT2 Profiler focused qPCR arrays and pathway analysis evaluating associations between human TJ and antiviral response were performed to identify potential interactions and pathways between genes of interests. Results: HRV-1B infection affected viability that was both time and TCID⁵⁰ dependent. Significant increases in apoptosis and viral replication post-infection correlated with viral titer. Viral infection significantly decreased claudin-1 protein expression at the lower TCID⁵⁰, while a significant decrease in all three TJ protein expressions occurred at higher TCID⁵⁰. Decrease in protein expression was concomitant with significant increases in epithelial permeability of fluorescein isothiocynate labeled-dextran 4 and 20 kDa. Analysis of focused qPCR arrays demonstrated a significant decrease in ZO-1 gene expression. Furthermore, network analysis between human TJ and antiviral response genes revealed possible interactions and regulation of TJ genes via interleukin (IL)-15 in response to HRV-1B infection. Conclusion: HRV-1B infection directly alters human airway epithelial TJ expression leading to increased epithelial permeability potentially via an antiviral response of IL-15.]]> Sat 24 Mar 2018 07:39:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27531 Sat 24 Mar 2018 07:28:58 AEDT ]]>