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Home / Equine Research Bank / J Virol / An equine infectious anemia virus variant superinfects cells...
Journal of virology2008; 82(19); 9425-9432; doi: 10.1128/JVI.01142-08

An equine infectious anemia virus variant superinfects cells through novel receptor interactions.

Abstract: Wild-type strains of equine infectious anemia virus (EIAV) prevent superinfection of previously infected cells. A variant strain of virus that spontaneously arose during passage, EIAV(vMA-1c), can circumvent this mechanism in some cells, such as equine dermis (ED) cells, but not in others, such as equine endothelial cells. EIAV(vMA-1c) superinfection of ED cells results in a buildup of unintegrated viral DNA and rapid killing of the cell monolayer. Here, we examined the mechanism of resistance that is used by EIAV to prevent superinfection and explored the means by which EIAV(vMA-1c) overcomes this restriction. We found that the cellular receptor used by EIAV, equine lentivirus receptor 1 (ELR1), remains on the surface of cells chronically infected with EIAV, suggesting that wild-type EIAV interferes with superinfection by masking ELR1. The addition of soluble wild-type SU protein to the medium during infection blocked infection by wild-type strains of virus, implicating SU as the viral protein responsible for interfering with virion entry into previously infected cells. Additionally, interference of wild-type EIAV binding to ELR1 by the addition of either anti-ELR1 antibodies or the ELR1 ectodomain prevented entry of the wild-type strains of EIAV into two permissive cell populations. Many of these same interference treatments prevented EIAV(vMA-1c) infection of endothelial cells but only modestly affected the ability of EIAV(vMA-1c) to enter and kill previously infected ED cells. These findings indicate that EIAV(vMA-1c) retains the ability to use ELR1 for entry and suggest that this virus can interact with an additional, unidentified receptor to superinfect ED cells.
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Publication Date: 2008-07-30 PubMed ID: 18667522PubMed Central: PMC2546952DOI: 10.1128/JVI.01142-08Google 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.

This research investigates how a variant strain of Equine Infectious Anemia virus (EIAV) is able to infect cells that are already infected with the virus, a phenomenon known as ‘superinfection’. The study finds that this variant strain, EIAV(vMA-1c), achieves superinfection by interacting with an unidentified additional receptor in certain types of cells, suggesting a novel mechanism adopted by the virus.

Background and Objective

  • The study began with the understanding that wild-type (naturally occurring) strains of EIAV usually block superinfection in previously affected cells. This prevention is believed to be due to the virus’ ability to mask the equine lentivirus receptor 1 (ELR1), which EIAV uses to enter cells.
  • The researchers were intrigued by a variant strain of the virus, EIAV(vMA-1c), that arose spontaneously and was observed to override this block in certain cell types, leading to their superinfection.
  • The aim of the research was to examine how wild-type EIAV prevents superinfection, and determine how EIAV(vMA-1c) was able to overcome this barrier.

Findings

  • The cellular receptor used by EIAV, ELR1, was found to be present on the surface of cells chronically infected with EIAV, indicating that wild-type EIAV’s ability to prevent superinfection works by masking ELR1.
  • It was observed that adding soluble wild-type SU protein during infection blocked the infection by wild-type strains, implicating SU as the viral protein responsible for blocking virion entry into already infected cells.
  • Interference treatments such as anti-ELR1 antibodies or the ELR1 ectodomain that blocked wild-type EIAV from binding to ELR1 also blocked virus entry in permissive cell populations.
  • Interestingly, these interference treatments only slightly affected EIAV(vMA-1c)’s ability to enter previously infected cells, suggesting that EIAV(vMA-1c) uses ELR1 for entry but may also interact with an additional, unidentified receptor to achieve superinfection within these cells.

Conclusion

  • The research supports the belief that EIAV employs a strategy to prevent superinfection in already infected cells by interacting with the ELR1 receptor.
  • EIAV(vMA-1c)’s ability to overcome this blockage and superinfect certain types of cells suggests that it may rely on an alternative receptor, beyond ELR1, for this purpose.
  • Further research is needed to identify this additional receptor used by EIAV(vMA-1c) for superinfection and to explore its potential implications for the progression and treatment of EIAV infections.

Cite This Article

APA
Brindley MA, Zhang B, Montelaro RC, Maury W. (2008). An equine infectious anemia virus variant superinfects cells through novel receptor interactions. J Virol, 82(19), 9425-9432. https://doi.org/10.1128/JVI.01142-08

Publication

Journal of virology
ISSN: 1098-5514
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 82
Issue: 19
Pages: 9425-9432

Researcher Affiliations

Brindley, Melinda A
  • 3-612 Bowen Science Bldg., Dept. Microbiology, University of Iowa, Iowa City, IA 52242, USA.
Zhang, Baoshan
    Montelaro, Ronald C
      Maury, Wendy

        MeSH Terms

        • Animals
        • Cell Line
        • Culture Media / metabolism
        • DNA, Viral / genetics
        • Dermis / virology
        • Fibroblasts / metabolism
        • Horses
        • Humans
        • Hydrogen-Ion Concentration
        • Infectious Anemia Virus, Equine / genetics
        • Infectious Anemia Virus, Equine / metabolism
        • Kinetics
        • Membrane Glycoproteins / metabolism
        • Phenotype
        • RNA, Small Interfering / metabolism
        • Receptors, Virus / metabolism
        • Viral Envelope Proteins / metabolism

        Grant Funding

        • 9R56 AI07326 / NIAID NIH HHS
        • T32 A1007533 / PHS HHS

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        Citations

        This article has been cited 5 times.
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