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. 2004 Feb;10(2):317-9.
doi: 10.3201/eid1002.030482.

Interferon-beta 1a and SARS coronavirus replication

Lisa E Hensley  1 , Lisa E Fritz, Peter B Jahrling, Christopher L Karp, John W Huggins, Thomas W Geisbert
Affiliations

Interferon-beta 1a and SARS coronavirus replication

Lisa E Hensley et al. Emerg Infect Dis. 2004 Feb.

Abstract

A global outbreak of severe acute respiratory syndrome (SARS) caused by a novel coronavirus began in March 2003. The rapid emergence of SARS and the substantial illness and death it caused have made it a critical public health issue. Because no effective treatments are available, an intensive effort is under way to identify and test promising antiviral drugs. Here, we report that recombinant human interferon-beta 1a potently inhibits SARS coronavirus replication in vitro.

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Figures

Figure 1
Figure 1
Interferon (IFN)-β 1a inhibition of SARS-CoV replication in Vero E-6 cells. Top panels, Vero E-6 cells were incubated in the absence (-▲-) or presence of IFN-β 1a added 24 h before infection with the Tor2 (left) or Tor7 (right) isolate of SARS Co-V. Bottom panels, Vero E-6 cells were incubated in the absence (-▲-) or presence of IFN-β 1a added 1 h after infection with the Tor2 (left) or Tor7 (right) isolate of SARS Co-V. Three concentrations of IFN-β 1a were employed for both studies: 5,000 IU/mL (-□-), 50,000 IU/mL (-■-), 500,000 IU/mL (-■-) Samples of overlying media were collected at 24, 48, and 72 h postinfection and analyzed by plaque assay on Vero E-6 cells.
Figure 2
Figure 2
Interferon (IFN)-β 1a inhibition of SARS-CoV cytopathicity in Vero E-6 cells. Vero E-6 cells were infected with the Tor2 isolate of SARS-CoV and incubated for 72 h in the absence (left panel) or presence (right panel) of 500,000 IU of recombinant human IFN-β 1a. Cell rounding and detachment were prominent in the absence of IFN-β 1a. Minimal cell rounding or death was noted in the intact monolayer at 72 h postinoculation in the presence of IFN-β 1a (note: IFN-β 1a administered 1 h postinfection).
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