SARS coronavirus induces apoptosis in Vero E6 Cells

Severe acute respiratory syndrome (SARS) is an emerging infectious disease. Its etiological agent has been convincingly identified as a new member of family Coronaviridae (SARS‐CoV). It causes serious damage to the respiratory system yet the mechanism is not clear. Infection‐induced apoptosis or nec...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of medical virology 2004-07, Vol.73 (3), p.323-331
Hauptverfasser: Yan, Huimin, Xiao, Gengfu, Zhang, Jiamin, Hu, Yuanyang, Yuan, Fang, Cole, David K., Zheng, Congyi, Gao, George F.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Severe acute respiratory syndrome (SARS) is an emerging infectious disease. Its etiological agent has been convincingly identified as a new member of family Coronaviridae (SARS‐CoV). It causes serious damage to the respiratory system yet the mechanism is not clear. Infection‐induced apoptosis or necrosis is suspected but no direct evidence for this yet exists. To date, Vero E6 cells are the only cell line that could be used to replicate the virus with obvious CPE (cytopathic effect) in vitro. It is known for some viruses (including members of family Coronaviridae) that CPE can be caused either by virus‐induced apoptosis (active death) or cell necrosis (passive death). In this study, we examined the apoptosis in the SARS‐CoV infected Vero E6 cells. Indeed, the results do show that the CPE was induced by apoptosis rather than necrosis, shown by typical DNA fragmentation, through the existence of apoptotic bodies and swollen mitochondria. This observation has some implications for the SARS‐CoV pathogenicity: SARS‐CoV does induce apoptosis in cell cultures and might have the same effect in vivo, responsible for the severe damage of the respiratory system. J. Med. Virol. 73:323–331, 2004. © 2004 Wiley‐Liss, Inc.
ISSN:0146-6615
1096-9071
DOI:10.1002/jmv.20094