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Journal of Virology, May 2009, p. 4216-4226, Vol. 83, No. 9
0022-538X/09/$08.00+0 doi:10.1128/JVI.02436-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Cantoblanco, Madrid, Spain,1 Departamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid (UAM), Cantoblanco, Madrid, Spain,2 Centro de Investigación en Sanidad Animal, INIA, Valdeolmos, Madrid, Spain3
Received 26 November 2008/ Accepted 8 February 2009
We performed a comparative analysis of the internalization mechanisms used by three viruses causing important vesicular diseases in animals. Swine vesicular disease virus (SVDV) internalization was inhibited by treatments that affected clathrin-mediated endocytosis and required traffic through an endosomal compartment. SVDV particles were found in clathrin-coated pits by electron microscopy and colocalized with markers of early endosomes by confocal microscopy. SVDV infectivity was significantly inhibited by drugs that raised endosomal pH. When compared to foot-and-mouth disease virus (FMDV), which uses clathrin-mediated endocytosis, the early step of SVDV was dependent on the integrity of microtubules. SVDV-productive endocytosis was more sensitive to plasma membrane cholesterol extraction than that of FMDV, and differential cell signaling requirements for virus infection were also found. Vesicular stomatitis virus, a model virus internalized by clathrin-mediated endocytosis, was included as a control of drug treatments. These results suggest that different clathrin-mediated routes are responsible for the internalization of these viruses.
Published ahead of print on 18 February 2009.
Dedicated to the memory of Rosario Armas-Portela.
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