Journalartikel
Autorenliste: Spiegel, M; Pichlmair, A; Martínez-Sobrido, L; Cros, J; García-Sastre, A; Haller, O; Weber, F
Jahr der Veröffentlichung: 2005
Seiten: 2079-2086
Zeitschrift: Journal of Virology
Bandnummer: 79
Heftnummer: 4
ISSN: 0022-538X
eISSN: 1098-5514
DOI Link: https://doi.org/10.1128/JVI.79.4.2079-2086.2005
Verlag: American Society for Microbiology
Abstract:
Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. We and others have previously shown that the replication of SARS-CoV can be suppressed by exogenously added interferon (IFN), a cytokine which is normally synthesized by cells as a reaction to virus infection. Here, we demonstrate that SARS-CoV escapes IFN-mediated growth inhibition by preventing the induction of IFN-beta. In SARS-CoV-infected cells, no endogenous IFN-beta transcripts and no IFN-beta promoter activity were detected. Nevertheless, the transcription factor interferon regulatory factor 3 (IRF-3), which is essential for IFN-beta promoter activity, was transported from the cytoplasm to the nucleus early after infection with SARS-CoV. However, at a later time point in infection, IRF-3 was again localized in the cytoplasm. By contrast, IRF-3 remained in the nucleus of cells infected with the IFN-inducing control virus Bunyamwera deINSs. Other signs of IRF-3 activation such as hyperphosphorylation, homodimer formation, and recruitment of the coactivator CREB-binding protein (CBP) were found late after infection with the control virus but not with SARS-CoV. Our data suggest that nuclear transport of IRF-3 is an immediate-early reaction to virus infection and may precede its hyperphosphorylation, homodimer formation, and binding to CBP. In order to escape activation of the IFN system, SARS-CoV appears to block a step after the early nuclear transport of IRF-3.
Zitierstile
Harvard-Zitierstil: Spiegel, M., Pichlmair, A., Martínez-Sobrido, L., Cros, J., García-Sastre, A., Haller, O., et al. (2005) Inhibition of Beta Interferon Induction by Severe Acute Respiratory Syndrome Coronavirus Suggests a Two-Step Model for Activation of Interferon Regulatory Factor 3, Journal of Virology, 79(4), pp. 2079-2086. https://doi.org/10.1128/JVI.79.4.2079-2086.2005
APA-Zitierstil: Spiegel, M., Pichlmair, A., Martínez-Sobrido, L., Cros, J., García-Sastre, A., Haller, O., & Weber, F. (2005). Inhibition of Beta Interferon Induction by Severe Acute Respiratory Syndrome Coronavirus Suggests a Two-Step Model for Activation of Interferon Regulatory Factor 3. Journal of Virology. 79(4), 2079-2086. https://doi.org/10.1128/JVI.79.4.2079-2086.2005