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Journal of Virology, August 2006, p. 7500-7509, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.02452-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Entry of Feline Calicivirus Is Dependent on Clathrin-Mediated Endocytosis and Acidification in Endosomes

Amanda D. Stuart* and T. David K. Brown

Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, United Kingdom

Received 22 November 2005/ Accepted 26 April 2006

Feline calicivirus is a major causative agent of respiratory disease in cats. It is also one of the few cultivatable members of Caliciviridae. We have examined the entry process of feline calicivirus (FCV). An earlier study demonstrated that acidification in endosomes may be required. We have confirmed this observation and expanded upon it, demonstrating, using drugs to inhibit the various endocytic pathways and dominant-negative mutants, that FCV infects cells via clathrin-mediated endocytosis. We have also observed that FCV permeabilizes cell membranes early during infection to allow the coentry of toxins such as {alpha}-sarcin. Inhibitors of endosome acidification such as chloroquine and bafilomycin A1 blocked this permeabilization event, demonstrating that acidification is required for uncoating of the genome and access to the cytoplasm.

* Corresponding author. Mailing address: Division of Virology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, United Kingdom. Phone: 01223 336918. Fax: 01223 336926. E-mail: ads35{at}mole.bio.cam.ac.uk.

Journal of Virology, August 2006, p. 7500-7509, Vol. 80, No. 15
0022-538X/06/$08.00+0     doi:10.1128/JVI.02452-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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Copyright © 2006 by the American Society for Microbiology. All rights reserved.