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|Title:||Antiviral Gene Expression during Human Coronavirus OC43 Infectio||Authors:||Meshal Samir Beidas||Supervisor:||Dr. Wassim Chehadeh||Keywords:||antiviral gene expression||Issue Date:||2018||Publisher:||Kuwait university - college of graduate studies||Abstract:||Human coronavirus OC43 (HCoV-OC43) is a respiratory virus that usually causes common cold. However, it has the potential to cause severe infection in young children and immunocompromised adults. Both SARS-CoV and MERS-CoV were shown to express proteins with the potential to evade early innate immune responses. However, the ability of HCoV-OC43 to antagonise the intracellular antiviral defences has not yet been investigated. The potential role of the HCoV-OC43 structural (M and N) and accessory proteins (ns2a and ns5a) in the alteration of antiviral gene expression was investigated in this study. HCoV-OC43 M, N, ns2a, and ns5a proteins were expressed in human embryonic kidney 293 (HEK-293) cells before challenging with Sendai virus (SeV). The Human Antiviral Response PCR array was used to profile the antiviral gene expression in HEK-293 cells, whereas the effect of HCoV-OC43 proteins on the transcriptional activation of antiviral response elements was assessed by measuring the levels of firefly luciferase expressed by a reporter vector under the control of interferon-stimulated response element (ISRE), interferon-beta (IFN-β) promoter, or nuclear factor kappa B response element (NF-κB-RE). Influenza A NS1 protein was used as a positive control for IFN antagonism. Over 30 genes were downregulated in the presence of one of the HCoV-OC43 proteins, e.g. mitogen-activated protein kinases, toll-like receptors, interferons, interleukins, and signalling transduction proteins. The transcriptional activity of ISRE, IFN-β promoter, and NF-κB-RE was significantly reduced in the presence of HCoV-OC43 ns2a, ns5a, M, or N protein, as there was a sharp fall in the firefly luciferase levels following the challenge of cells with SeV, IFN- or TNF-Our findings suggest that similarly to SARS-CoV and MERS-CoV, HCoV-OC43 has the ability to downregulate the transcription of genes critical for the activation of different antiviral signalling pathways. Further studies are needed to confirm the role of HCoV-OC43 structural and accessory proteins in antagonising antiviral gene expression.||URI:||http://hdl.handle.net/123456789/699|
|Appears in Programs:||0520 Microbiology (Ph.D.)|
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