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Volume 10, Number 2—February 2004
THEME ISSUE
2004 SARS Edition
Laboratory Study

Interferon-β 1a and SARS Coronavirus Replication

Lisa E. Hensley*, Elizabeth A. Fritz*, Peter B. Jahrling*Comments to Author , Christopher Karp†, John W. Huggins*, and Thomas W. Geisbert*
Author affiliations: *U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA; †Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA

Main Article

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).

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).

Main Article

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