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|Title:||MOLECULAR AND CELLULAR STUDY OF A NEWLY DISCOVERED HUMAN CARDIOVIRUS (SAFFOLD VIRUS - PENANG)||Authors:||XU YISHI||Keywords:||Saffold Virus, Cell death, Apoptosis, Cellular localization, Protein interactions||Issue Date:||18-Jan-2017||Citation:||XU YISHI (2017-01-18). MOLECULAR AND CELLULAR STUDY OF A NEWLY DISCOVERED HUMAN CARDIOVIRUS (SAFFOLD VIRUS - PENANG). ScholarBank@NUS Repository.||Abstract:||Saffold virus (SAFV), a newly discovered human cardiovirus of the Picornaviridae family, causes widespread infection among children as shown by previous seroprevalence studies. However, the link between SAFV infection and actual human disease remains unclear, and the research focusing on molecular and cellular aspects of SAFV is limited currently. The research reported in this thesis characterized SAFV-Penang from molecular and cellular aspects. The results showed that 1) SAFV could permissibly infect HEp-2, Vero, Neuro2A, NIH/3T3 and CHO-K1 cells; 2) the SAFV infection caused the host cells to undergo apoptosis, but the apoptotic activity in HEp-2 cells could not proceed to end-stage; 3) the SAFV 2B and 3C protein rather than the L protein, were responsible for the apoptotic activity caused by the SAFV infection; 4) most of the SAFV viral proteins under study were confined in the cytoplasm of HEp-2 and Vero cells, while the L protein was transferred to the nucleus in HEp-2 cells at the late stage of infection or transfection with related phosphorylation on the Theorine 58 of the L protein; 5) the SAFV L protein only interacts with Ran-GTPase in HEp-2 cells, but not in Vero cells, whereas the L protein of DA strain of TMEV interacts with Ran-GTPase in both HEp-2 and Vero cells. This study would contribute to the understanding of the mechanisms of SAFV infection, the virus-host interaction, and the roles of viral proteins during virus infection.||URI:||http://scholarbank.nus.edu.sg/handle/10635/135858|
|Appears in Collections:||Ph.D Theses (Open)|
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