Please use this identifier to cite or link to this item: https://doi.org/10.1038/emi.2014.15
Title: Saffold virus is able to productively infect primate and rodent cell lines and induces apoptosis in these cells
Authors: Xu, Y.
Victorio, C.B.L.
Ng, Q.
Tan, Y.J. 
Chua, K.B.
Keywords: Apoptosis
Cytopathic effect
Permissible cells
Saffold virus
Issue Date: 2014
Citation: Xu, Y., Victorio, C.B.L., Ng, Q., Tan, Y.J., Chua, K.B. (2014). Saffold virus is able to productively infect primate and rodent cell lines and induces apoptosis in these cells. Emerging Microbes and Infections 3 : -. ScholarBank@NUS Repository. https://doi.org/10.1038/emi.2014.15
Abstract: Saffold virus (SAFV), a newly discovered human cardiovirus of the Picornaviridae family, causes widespread infection among children, as shown by previous seroprevalence studies. To determine the host cell range of SAFV and its cytopathogenicity, eight mammalian cell lines that were available in the laboratory were screened for productive SAFV infection by a laboratory-adapted SAFV of genotype 3. Five of the cell lines (Neuro2A, CHO-K1, NIH/3T3, Vero and HEp-2) were found to be permissible. The time required for SAFV to induce complete lysis as a cytopathic effect (CPE) in these permissibly infected cells and the resultant end point virus titer differed for each cell type. HEp-2 exhibited the shortest time frame to reach full CPE compared to the others. All infected cell lines produced a high virus titer at 72 h post-infection. In addition to causing lytic cell death, SAFV also induced apoptotic cell death in host cells through both extrinsic and intrinsic pathways, although the apoptotic events in HEp-2 cells appeared to have been blocked between the early and late stages. In conclusion, laboratory-adapted SAFV is able to productively infect a number of mammalian cell lines and induce apoptosis in the infected host cells. However, apoptosis in HEp-2 cells is blocked before the end stage. © 2014 SSCC. All rights reserved.
Source Title: Emerging Microbes and Infections
URI: http://scholarbank.nus.edu.sg/handle/10635/109637
ISSN: 22221751
DOI: 10.1038/emi.2014.15
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