ArticleJournal of virology2008
Equine infectious anemia virus entry occurs through clathrin-mediated endocytosis.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Inactivating conditions of therapeutic mycobacteriophages.Microbiology spectrum · 2026Article
- Transcriptomic analysis of phage-mammalian cell interaction reveals diverse phage immunobarcodes.iScience · 2025Article
- Inactivating conditions of therapeutic mycobacteriophages.bioRxiv : the preprint server for biology · 2025Article
- Review
- Isolation-protocol, characterization, andFrontiers in veterinary science · 2024Article
- Acquisition and Exaptation of Endogenous Retroviruses in Mammalian Placenta.Biomolecules · 2023Review
- Intracellular Staphylococcus aureus Control by Virulent Bacteriophages within MAC-T Bovine Mammary Epithelial Cells.Antimicrobial agents and chemotherapy · 2017Article
- Transmembrane Domain Lengths Serve as Signatures of Organismal Complexity and Viral Transport Mechanisms.Scientific reports · 2016Article
- HIV-1 entry in SupT1-R5, CEM-ss, and primary CD4+ T cells occurs at the plasma membrane and does not require endocytosis.Journal of virology · 2014Article
- Retrovirus entry by endocytosis and cathepsin proteases.Advances in virology · 2012Article
- CD4-independent human immunodeficiency virus infection involves participation of endocytosis and cathepsin B.PloS one · 2011Article
- Interplay between HIV entry and transportin-SR2 dependency.Retrovirology · 2011Article
- The Tyro3 receptor kinase Axl enhances macropinocytosis of Zaire ebolavirus.Journal of virology · 2011Article
- The Role of Lipids in Retrovirus Replication.Viruses · 2010Article
- Inhibition of lentivirus replication by aqueous extracts of Prunella vulgaris.Virology journal · 2009Article
- Host cell factors and functions involved in vesicular stomatitis virus entry.Journal of virology · 2009Article
- An equine infectious anemia virus variant superinfects cells through novel receptor interactions.Journal of virology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.