Viral protein synthesis is required for Enterovirus 71 to induce apoptosis in human glioblastoma cells

Human glioblastoma cells (SF268) develop apoptosis, as characterized by DNA fragmentation and caspase activation, upon infection with Enterovirus 71 (EV71). To determine the step in virus replication that triggers apoptosis, the authors used ultraviolet (UV)-inactivated virus, inhibitors of protein...

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Published inJournal of neurovirology Vol. 14; no. 1; pp. 53 - 61
Main Authors Shih, Shin-Ru, Weng, Kuo-Feng, Stollar, Victor, Li, Mei-Ling
Format Journal Article
LanguageEnglish
Published New York Informa UK Ltd 01.01.2008
Springer-Verlag
Taylor & Francis
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ISSN1355-0284
1538-2443
1538-2443
DOI10.1080/13550280701798980

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Summary:Human glioblastoma cells (SF268) develop apoptosis, as characterized by DNA fragmentation and caspase activation, upon infection with Enterovirus 71 (EV71). To determine the step in virus replication that triggers apoptosis, the authors used ultraviolet (UV)-inactivated virus, inhibitors of protein and viral RNA synthesis, and chloroquine to block virus uncoating. Activation of caspase-3 was detected 24 h after infection with EV71 but not with UV-inactivated EV71. Apoptosis was inhibited when EV71-infected cells were treated with chloroquine, guanidine HCl, or cycloheximide. In summary, the authors studied the event(s) required to induce apoptosis in EV71-infected human glioblastoma cells, a subject much less studied than the possible role of viral proapoptotic genes, concluding that EV71 induces apoptosis in the infected SF268 cell in the presence of viral protein synthesis and virus replication, whereas virus adsorption, internalization, entry, uncoating, and viral RNA replication are all not required to trigger the apoptosis.
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ISSN:1355-0284
1538-2443
1538-2443
DOI:10.1080/13550280701798980