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Virus research2014; 195; 172-176; doi: 10.1016/j.virusres.2014.10.014

The haemagglutination activity of equine herpesvirus type 1 glycoprotein C.

Abstract: Equine herpesvirus type 1 (EHV-1) has haemagglutination (HA) activity toward equine red blood cells (RBCs), but the identity of its haemagglutinin is unknown. To identify the haemagglutinin of EHV-1, the major glycoproteins of EHV-1 were expressed in 293T cells, and the cells or cell lysates were mixed with equine RBCs. The results showed that only EHV-1 glycoprotein C (gC)-producing cells adsorbed equine RBCs, and that the lysate of EHV-1 gC-expressing cells agglutinated equine RBCs. EHV-1 lacking gC did not show HA activity. HA activity was inhibited by monoclonal antibodies (MAbs) specific for gC, but not by antibodies directed against other glycoproteins. In addition, HA activity was not inhibited by the addition of heparin. These results indicate that EHV-1 gC can bind equine RBCs irrespective of heparin, in contrast to other herpesvirus gC proteins.
Publication Date: 2014-10-23 PubMed ID: 25456403DOI: 10.1016/j.virusres.2014.10.014Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research sought to identify the component of the Equine herpesvirus type 1 (EHV-1) that causes haemagglutination, a process in which red blood cells clump together. The findings revealed that Glycoprotein C (gC) of EHV-1 is responsible for this action.

Research Objective and Methodology

  • The primary aim of this research was to find the haemagglutinin of the EHV-1. Haemagglutinin is a substance that causes red blood cells (RBCs) to stick together.
  • The researchers worked with the major glycoproteins of EHV-1. These proteins were expressed inside 293T cells, which were later mixed with equine red blood cells.

Research Findings

  • Through experimentation, the study showed that only cells producing EHV-1 glycoprotein C (gC) attracted equine red blood cells. Furthermore, equine RBCs were also clumped together by the lysate of EHV-1 gC-expressing cells.
  • In contrast, EHV-1 that lacked gC did not demonstrate any haemagglutination activity.
  • The researchers also found that the action of haemagglutination was stopped by monoclonal antibodies (MAbs) that were specific to gC. However, antibodies directed against other glycoproteins did not have this effect.

Further Observations and Conclusions

  • Heparin, a commonly used anticoagulant, did not inhibit haemagglutination activity in this experiment.
  • The above outcomes indicate that EHV-1 gC has the ability to bind equine RBCs whether heparin is present or not. This behaviour contrasts with other herpesvirus gC proteins.
  • In conclusion, the study identified EHV-1 glycoprotein C as the agent of haemagglutination activity in relation to equine red blood cells.

Cite This Article

APA
Andoh K, Hattori S, Mahmoud HY, Takasugi M, Shimoda H, Bannai H, Tsujimura K, Matsumura T, Kondo T, Kirisawa R, Mochizuki M, Maeda K. (2014). The haemagglutination activity of equine herpesvirus type 1 glycoprotein C. Virus Res, 195, 172-176. https://doi.org/10.1016/j.virusres.2014.10.014

Publication

ISSN: 1872-7492
NlmUniqueID: 8410979
Country: Netherlands
Language: English
Volume: 195
Pages: 172-176
PII: S0168-1702(14)00419-5

Researcher Affiliations

Andoh, Kiyohiko
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Hattori, Shiho
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Mahmoud, Hassan Y A H
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Takasugi, Maaya
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Shimoda, Hiroshi
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan.
Bannai, Hiroshi
  • Molecular Biology Division, Epizootic Research Center, Equine Research Institute, Japan Racing Association, Shimotsuke, Tochigi 329-0412, Japan.
Tsujimura, Koji
  • Molecular Biology Division, Epizootic Research Center, Equine Research Institute, Japan Racing Association, Shimotsuke, Tochigi 329-0412, Japan.
Matsumura, Tomio
  • Molecular Biology Division, Epizootic Research Center, Equine Research Institute, Japan Racing Association, Shimotsuke, Tochigi 329-0412, Japan.
Kondo, Takashi
  • Molecular Biology Division, Epizootic Research Center, Equine Research Institute, Japan Racing Association, Shimotsuke, Tochigi 329-0412, Japan.
Kirisawa, Rikio
  • Department of Veterinary Virology, Rakuno Gakuen University, Ebetsu, Hokkaido 069-0836, Japan.
Mochizuki, Masami
  • Laboratory of Emerging Infectious Diseases, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan.
Maeda, Ken
  • Laboratory of Veterinary Microbiology, Joint Faculty of Veterinary Medicine, Yamaguchi University, 1677-1 Yoshida, Yamaguchi 753-8515, Japan. Electronic address: kmaeda@yamaguchi-u.ac.jp.

MeSH Terms

  • Animals
  • Erythrocytes / drug effects
  • Hemagglutination
  • Hemagglutinins / metabolism
  • Herpesvirus 1, Equid / physiology
  • Horses
  • Viral Envelope Proteins / metabolism

Citations

This article has been cited 2 times.
  1. Laval K, Poelaert KCK, Van Cleemput J, Zhao J, Vandekerckhove AP, Gryspeerdt AC, Garré B, van der Meulen K, Baghi HB, Dubale HN, Zarak I, Van Crombrugge E, Nauwynck HJ. The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1.. Front Microbiol 2021;12:662686.
    doi: 10.3389/fmicb.2021.662686pubmed: 33746936google scholar: lookup
  2. Spiesschaert B, Goldenbogen B, Taferner S, Schade M, Mahmoud M, Klipp E, Osterrieder N, Azab W. Role of gB and pUS3 in Equine Herpesvirus 1 Transfer between Peripheral Blood Mononuclear Cells and Endothelial Cells: a Dynamic In Vitro Model.. J Virol 2015 Dec;89(23):11899-908.
    doi: 10.1128/JVI.01809-15pubmed: 26378176google scholar: lookup