This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johannsdottir, H. K.
Right arrow Articles by Helenius, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johannsdottir, H. K.
Right arrow Articles by Helenius, A.

 Previous Article  |  Next Article 

Journal of Virology, January 2009, p. 440-453, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01864-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Host Cell Factors and Functions Involved in Vesicular Stomatitis Virus Entry{triangledown}

Hrefna Kristin Johannsdottir,1 Roberta Mancini,1 Jurgen Kartenbeck,2 Lea Amato,1 and Ari Helenius1*

Institute of Biochemistry, ETH Zurich, Schafmattstrasse 18, CH-8093 Zurich, Switzerland,1 Division of Cell Biology, German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany2

Received 4 September 2008/ Accepted 19 October 2008

Vesicular stomatitis virus (VSV) is an animal virus that based on electron microscopy and its dependence on acidic cellular compartments for infection is thought to enter its host cells in a clathrin-dependent manner. The exact cellular mechanism, however, is largely unknown. In this study, we characterized the entry kinetics of VSV and elucidated viral requirements for host cell factors during infection in HeLa cells. We found that endocytosis of VSV was a fast process with a half time of 2.5 to 3 min and that acid activation occurred within 1 to 2 min after internalization in early endosomes. The majority of viral particles were endocytosed in a clathrin-based, dynamin-2-dependent manner. Although associated with some of the surface-bound viruses, the classical adaptor protein complex AP-2 was not required for infection. Time-lapse microscopy revealed that the virus either entered preformed clathrin-coated pits or induced de novo formation of pits. Dynamin-2 was recruited to plasma membrane-confined virus particles. Thus, VSV can induce productive internalization by exploiting a specific combination of the clathrin-associated proteins and cellular functions.

* Corresponding author. Mailing address: Institute of Biochemistry, ETH Zurich, Schafmattstrasse 18, CH-8093 Zurich, Switzerland. Phone: 41 44 632 68 17. Fax: 41 44 632 12 69. E-mail: ari.helenius{at}bc.biol.ethz.ch

{triangledown} Published ahead of print on 29 October 2008.

Journal of Virology, January 2009, p. 440-453, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01864-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»