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Equine Infectious Anemia Virus Entry Occurs through Clathrin-Mediated Endocytosis
Journal article   Open access   Peer reviewed

Equine Infectious Anemia Virus Entry Occurs through Clathrin-Mediated Endocytosis

Melinda A Brindley and Wendy Maury
Journal of virology, Vol.82(4), pp.1628-1637
02/2008
DOI: 10.1128/JVI.01754-07
PMCID: PMC2258727
PMID: 18057237
url
https://doi.org/10.1128/JVI.01754-07View
Published (Version of record) Open Access

Abstract

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, 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, 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.
 Virus-Cell Interactions

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