DOI: 10.1128/JVI.79.16.10826-10829.2005
ABSTRACT
Cellular mechanisms of bovine viral diarrhea virus (BVDV) entry in MDBK cells were investigated. Chloroquine, bafilomycin A1, or ammonium chloride inhibited BVDV infection, indicating that an acidic endosomal pH is required for BVDV entry. The tyrosine kinase inhibitor genistein partially inhibited BVDV infection at a postentry step, whereas BVDV entry was strongly inhibited by chlorpromazine or by the overexpression of a dominant-negative form of EPS15, a protein essential for the formation of clathrin-coated vesicles at the plasma membrane. Together, these data indicate that BVDV infection requires an active clathrin-dependent endocytic pathway.
FOOTNOTES
- Received 13 December 2004.
- Accepted 21 May 2005.
- ↵*Corresponding author. Mailing address: Unité Hépatite C, CNRS-UPR2511, Institut Pasteur de Lille, 1 rue Calmette, BP 447, 59021 Lille Cedex, France. Phone: (33) 3 20 87 10 27. Fax: (33) 3 20 87 12 01. E-mail: yves.rouille{at}ibl.fr.
- American Society for Microbiology
