JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
JVI.01754-07v1
82/4/1628    most recent
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
Google Scholar
Right arrow Articles by Brindley, M. A.
Right arrow Articles by Maury, W.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brindley, M. A.
Right arrow Articles by Maury, W.
Journal of Virology, February 2008, p. 1628-1637, Vol. 82, No. 4
0022-538X/08/$08.00+0     doi:10.1128/JVI.01754-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Equine Infectious Anemia Virus Entry Occurs through Clathrin-Mediated Endocytosis{triangledown}

Melinda A. Brindley and Wendy Maury*

Department of Microbiology, University of Iowa, Iowa City, Iowa 52242

Received 10 August 2007/ Accepted 26 November 2007

Entry of wild-type lentivirus equine infectious anemia virus (EIAV) into cells requires a low-pH step. This low-pH constraint implicates endocytosis in EIAV entry. To identify the endocytic pathway involved in EIAV entry, we examined the entry requirements for EIAV into two different cells: equine dermal (ED) cells and primary equine endothelial cells. We investigated the entry mechanism of several strains of EIAV and found that both macrophage-tropic and tissue culture-adapted strains utilize clathrin-coated pits for entry. In contrast, a superinfecting strain of EIAV, EIAVvMA-1c, utilizes two mechanisms of entry. In cells such as ED cells that EIAVvMA-1c is able to superinfect, viral entry is pH independent and appears to be mediated by plasma membrane fusion, whereas in cells where no detectable superinfection occurs, EIAVvMA-1c entry that is low-pH dependent occurs through clathrin-coated pits in a manner similar to wild-type virus. Regardless of the mechanism of entry being utilized, the internalization kinetics of EIAV is rapid with 50% of cell-associated virions internalizing within 60 to 90 min. Cathepsin inhibitors did not prevent EIAV entry, suggesting that the low-pH step required by wild-type EIAV is not required to activate cellular cathepsins.

* Corresponding author. Mailing address: 3-612 Bowen Science Bldg., Dept. Microbiology, University of Iowa, Iowa City, IA 52242. Phone: (319) 335-8021. Fax: (319) 335-9006. E-mail: wendy-maury{at}uiowa.edu

{triangledown} Published ahead of print on 5 December 2007.

Journal of Virology, February 2008, p. 1628-1637, Vol. 82, No. 4
0022-538X/08/$08.00+0     doi:10.1128/JVI.01754-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2008 by the American Society for Microbiology. All rights reserved.