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Journal of Virology, March 2007, p. 2995-2998, Vol. 81, No. 6
0022-538X/07/$08.00+0 doi:10.1128/JVI.02486-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Pathobiological Sciences, School of Veterinary Medicine, University of WisconsinMadison, Madison, Wisconsin,1 United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland,2 Uniformed Services University of the Health Sciences, Bethesda, Maryland,3 Special Pathogens Program, National Microbiology Laboratory, Public Health Agency of Canada, and Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada,4 Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan5
Received 12 November 2006/ Accepted 19 December 2006
Enveloped viruses often require cleavage of a surface glycoprotein by a cellular endoprotease such as furin for infectivity and virulence. Previously, we showed that Ebola virus glycoprotein does not require the furin cleavage motif for virus replication in cell culture. Here, we show that there are no appreciable differences in disease progression, hematology, serum biochemistry, virus titers, or lethality in nonhuman primates infected with an Ebola virus lacking the furin recognition sequence compared to those infected with wild-type virus. We conclude that glycoprotein cleavage by subtilisin-like endoproteases is not critical for Ebola virus infectivity and virulence in nonhuman primates.
Published ahead of print on 17 January 2007.
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