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Home / Equine Research Bank / J Virol / Equine infectious anemia virus entry occurs through clathrin...
Journal of virology2007; 82(4); 1628-1637; doi: 10.1128/JVI.01754-07

Equine infectious anemia virus entry occurs through clathrin-mediated endocytosis.

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.
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Publication Date: 2007-12-05 PubMed ID: 18057237PubMed Central: PMC2258727DOI: 10.1128/JVI.01754-07Google Scholar: Lookup
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Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The study investigates how the equine infectious anemia virus (EIAV), a type of lentivirus, enters cells. The researchers discovered that various strains of EIAV, including both macrophage-tropic and tissue-culture adapted strains, use clathrin-coated pits for cell entry. Another strain, EIAV(vMA-1c), could enter cells through two different mechanisms.

Virus and Cell Types

  • The study focused on a lentivirus known as EIAV, which is known to require a low-pH environment to enter a cell.
  • The entry process of this virus was investigated in different cell types, including equine dermal (ED) cells and primary equine endothelial cells.

Study Findings

  • The researchers found that both macropage-tropic and tissue culture-adapted strains of the virus used clathrin-coated pits, structures on the surface of cells involved in the process of endocytosis, for entering the cells.
  • A different strain of the virus, EIAV(vMA-1c), demonstrated two distinct entry mechanisms. One involved plasma membrane fusion in certain cell types where the strain could superinfect. This process was pH-independent, contrary to what is usually required for EIAV.
  • The same EIAV(vMA-1c) strain also utilized a mechanism similar to the wild-type virus in cells where it couldn’t superinfect. This involved low-pH-dependent entry through clathrin-coated pits.
  • Regardless of which method the virus used to enter the cell, the internalization process was quick, with 50% of the attached viruses entering within 60 to 90 minutes.

Implications

  • The researchers noted that using cathepsin inhibitors did not prevent EIAV from entering cells. This suggests that the low-pH step required for most EIAV strains is not necessary to activate cellular cathepsins, enzymes in the cell that are typically involved in intracellular protein breakdown.
  • Understanding the different mechanisms viruses use to enter cells can provide valuable insights that could lead to the development of better antiviral therapies.

Cite This Article

APA
Brindley MA, Maury W. (2007). Equine infectious anemia virus entry occurs through clathrin-mediated endocytosis. J Virol, 82(4), 1628-1637. https://doi.org/10.1128/JVI.01754-07

Publication

Journal of virology
ISSN: 1098-5514
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 82
Issue: 4
Pages: 1628-1637

Researcher Affiliations

Brindley, Melinda A
  • Department of Microbiology, University of Iowa, Iowa City, Iowa 52242, USA.
Maury, Wendy

    MeSH Terms

    • Actins / metabolism
    • Animals
    • Cathepsins / antagonists & inhibitors
    • Cathepsins / metabolism
    • Cell Line
    • Cholesterol / metabolism
    • Clathrin / metabolism
    • Clathrin-Coated Vesicles / virology
    • Dynamin I / metabolism
    • Endocytosis / drug effects
    • Hydrogen-Ion Concentration
    • Infectious Anemia Virus, Equine / physiology
    • Membrane Fusion
    • Membrane Microdomains / virology
    • Protease Inhibitors / pharmacology
    • Virus Internalization / drug effects

    Grant Funding

    • R21 AI064526 / NIAID NIH HHS

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    Citations

    This article has been cited 11 times.
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