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Home / Equine Research Bank / J Virol / Equine Arteritis Virus Uses Equine CXCL16 as an Entry Recept...
Journal of virology2016; 90(7); 3366-3384; doi: 10.1128/JVI.02455-15

Equine Arteritis Virus Uses Equine CXCL16 as an Entry Receptor.

Abstract: Previous studies in our laboratory have identified equine CXCL16 (EqCXCL16) to be a candidate molecule and possible cell entry receptor for equine arteritis virus (EAV). In horses, the CXCL16 gene is located on equine chromosome 11 (ECA11) and encodes a glycosylated, type I transmembrane protein with 247 amino acids. Stable transfection of HEK-293T cells with plasmid DNA carrying EqCXCL16 (HEK-EqCXCL16 cells) increased the proportion of the cell population permissive to EAV infection from <3% to almost 100%. The increase in permissiveness was blocked either by transfection of HEK-EqCXCL16 cells with small interfering RNAs (siRNAs) directed against EqCXCL16 or by pretreatment with guinea pig polyclonal antibody against EqCXCL16 protein (Gp anti-EqCXCL16 pAb). Furthermore, using a virus overlay protein-binding assay (VOPBA) in combination with far-Western blotting, gradient-purified EAV particles were shown to bind directly to the EqCXCL16 protein in vitro. The binding of biotinylated virulent EAV strain Bucyrus at 4°C was significantly higher in HEK-EqCXCL16 cells than nontransfected HEK-293T cells. Finally, the results demonstrated that EAV preferentially infects subpopulations of horse CD14(+) monocytes expressing EqCXCL16 and that infection of these cells is significantly reduced by pretreatment with Gp anti-EqCXCL16 pAb. The collective data from this study provide confirmatory evidence that the transmembrane form of EqCXCL16 likely plays a major role in EAV host cell entry processes, possibly acting as a primary receptor molecule for this virus. Objective: Outbreaks of EVA can be a source of significant economic loss for the equine industry from high rates of abortion in pregnant mares, death in young foals, establishment of the carrier state in stallions, and trade restrictions imposed by various countries. Similar to other arteriviruses, EAV primarily targets cells of the monocyte/macrophage lineage, which, when infected, are believed to play a critical role in EVA pathogenesis. To this point, however, the host-specified molecules involved in EAV binding and entry into monocytes/macrophages have not been identified. Identification of the cellular receptors for EAV may provide insights to design antivirals and better prophylactic reagents. In this study, we have demonstrated that EqCXCL16 acts as an EAV entry receptor in EAV-susceptible cells, equine monocytes. These findings represent a significant advance in our understanding of the fundamental mechanisms associated with the entry of EAV into susceptible cells.
Copyright © 2016, American Society for Microbiology. All Rights Reserved.
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Publication Date: 2016-01-13 PubMed ID: 26764004PubMed Central: PMC4794689DOI: 10.1128/JVI.02455-15Google Scholar: Lookup
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  • U.S. Gov't
  • Non-P.H.S.

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 research investigates the role of equine CXCL16 (EqCXCL16) as an entry receptor for the equine arteritis virus (EAV), revealing that this molecule is likely a major component in EAV’s host cell entry process, thus deepening our understanding of how EAV infects its host cells.

Objective and Significance

  • The objective of this research was to determine whether EqCXCL16 facilitates the entry of EAV into sensitive cells, specifically equine monocytes.
  • The findings have great economic significance, as the EAV is central to outbreaks causing reduced fertility, death in young foals, and trade restrictions – all causing substantial losses in the equine industry.
  • Identifying EAV’s cellular receptors could pave the way to designing effective antivirals and prophylactic agents.
  • The study further contributes to understanding the pathogenesis of arterivirus infections, which primarily target cells of the monocyte/macrophage lineage.

Research Process and Findings

  • The researchers found that stable transfection of HEK-293T cells with EqCXCL16 significantly increased their susceptibility to EAV infection from less than 3% to almost 100%.
  • This increased susceptibility was prevented by either transfecting the HEK-EqCXCL16 cells with siRNAs that would “silence” EqCXCL16, or by pretreating the cells with a guinea pig-derived antibody against the EqCXCL16 protein.
  • Using a combination of a virus overlay protein-binding assay and far-Western blotting, the researchers were able to show that EAV particles directly bind to the EqCXCL16 protein in vitro.
  • At a low temperature (4°C), the binding of a biotinylated virulent EAV strain to HEK-EqCXCL16 cells was significantly higher than to non-transfected cells, indicating that the virus’s entry into the cells was facilitated by EqCXCL16.
  • The researchers also discovered that EAV is more likely to infect populations of horse CD14(+) monocytes expressing EqCXCL16, and that infection rates of these cells dropped dramatically when they were pretreated with the antibody against EqCXCL16.

Conclusion

  • The results of this research substantiate the hypothesis that the transmembrane form of EqCXCL16 plays a significant role in EAV’s ability to enter host cells and may act as the primary receptor molecule for this virus.
  • This study represents a major breakthrough in unraveling the mechanisms underlying EAV’s entry into susceptible cells, and could potentially inform the development of preventive measures and treatments against infections caused by this virus.

Cite This Article

APA
Sarkar S, Chelvarajan L, Go YY, Cook F, Artiushin S, Mondal S, Anderson K, Eberth J, Timoney PJ, Kalbfleisch TS, Bailey E, Balasuriya UB. (2016). Equine Arteritis Virus Uses Equine CXCL16 as an Entry Receptor. J Virol, 90(7), 3366-3384. https://doi.org/10.1128/JVI.02455-15

Publication

Journal of virology
ISSN: 1098-5514
NlmUniqueID: 0113724
Country: United States
Language: English
Volume: 90
Issue: 7
Pages: 3366-3384

Researcher Affiliations

Sarkar, Sanjay
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Chelvarajan, Lakshman
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Go, Yun Young
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Cook, Frank
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Artiushin, Sergey
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Mondal, Shankar
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Anderson, Kelsi
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Eberth, John
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Timoney, Peter J
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Kalbfleisch, Theodore S
  • Center for Environmental Genomics and Integrative Biology, University of Louisville, Louisville, Kentucky, USA.
Bailey, Ernest
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA.
Balasuriya, Udeni B R
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky, USA ubalasuriya@uky.edu.

MeSH Terms

  • Amino Acid Sequence
  • Animals
  • Antibodies, Viral / immunology
  • Arterivirus Infections / virology
  • Base Sequence
  • Cell Line
  • Chemokines, CXC / antagonists & inhibitors
  • Chemokines, CXC / genetics
  • Chemokines, CXC / physiology
  • Cricetinae
  • Equartevirus / genetics
  • Equartevirus / physiology
  • Guinea Pigs
  • HEK293 Cells
  • Horse Diseases / virology
  • Horses
  • Host Specificity / genetics
  • Humans
  • RNA Interference
  • RNA, Small Interfering / genetics
  • Rabbits
  • Receptors, Virus / genetics
  • Receptors, Virus / metabolism
  • Sequence Analysis, DNA
  • Virus Attachment
  • Virus Internalization

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Citations

This article has been cited 15 times.
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