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J. Virol. doi:10.1128/JVI.01754-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

EQUINE INFECTIOUS ANEMIA VIRUS ENTRY OCCURS THROUGH CLATHRIN-MEDIATED ENDOCYTOSIS

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

^* To whom correspondence should be addressed. Email: wendy-maury{at}uiowa.edu.

	Abstract

Entry of wild-type lentivirus equine infectious anemia virus (EIAV) into cells requires a low-pH step (10, 31). 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 investigate the entry mechanism of several strains of EIAV and find that both macrophage tropic and tissue culture adapted strains utilizes clathrin coated pits for entry. In contrast, a superinfecting strain of EIAV, EIAV_vMA-1c,utilizes two mechanisms of entry. In cells such as ED cells that EIAV_vMA-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, EIAV_vMA-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, internalization kinetics of EIAVis rapid with 50% of cell associated virions internalizing within 60-90 minutes. 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.