Host cell tropism of equine herpesviruses: glycoprotein D of EHV-1 enables EHV-4 to infect a non-permissive cell line.
Abstract: Equine herpesviruses 1 and 4 (EHV-1 and EHV-4) cause equine respiratory disease worldwide. However, only EHV-1 is a cause of abortion and neurological disease, despite the two viruses having all 76 genes in common. In addition EHV-1 has a broader host range in cell culture than EHV-4, as exemplified by the rabbit kidney (RK) cell line that is permissive for EHV-1, but not for EHV-4. Here we describe that when EHV-4 produced in equine cells was inoculated onto RK cells expressing glycoprotein D of EHV-1 (RKgD1), infection developed as clusters of rounded cells, and this infectivity could be passaged in RKgD1 cells. The progeny virus could also infect single RK cells, consistent with EHV-4 acquiring EHV1 gD from the complementing cell line. No such infection was observed for EHV-4 in RK cells expressing EHV-1 glycoprotein C. The results are consistent with gD homologues being major determinants of host cell tropism and raise the possibility that gD may be a factor in the differential pathogenicity of EHV-1 and EHV-4.
Publication Date: 2006-12-15 PubMed ID: 17171298DOI: 10.1007/s00705-006-0885-xGoogle Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research study explores why Equine Herpesviruses 1 and 4 (EHV-1 and EHV-4) – which share similar genetic structures – affect horses differently. The researchers found that the glycoprotein D (gD) of EHV-1 enables EHV-4 to infect non-permissive cells, suggesting a possible role in the differing pathogenicity of these two viruses.
Background of the Study
- The research starts from the premise that both EHV-1 and EHV-4 viruses are responsible for respiratory disease in horses around the globe.
- However, a critical difference is observed in their manifestation. EHV-1 has been identified as a cause for abortion and neurological disease, while EHV-4 does not have such implications. This is intriguing to researchers, given both viruses share all 76 genes.
- Furthermore, EHV-1 also shows a broader range of host targets in cell cultures as compared to EHV-4.
Research Methodology
- The researchers used the rabbit kidney (RK) cell line, which is permissive, meaning, capable of being infected by EHV-1, but not by EHV-4, as an illustrative example.
- In their method, EHV-4, which is produced in horse cells, was inoculated onto the RK cells expressing EHV-1’s glycoprotein D (gD), identified within the study as RKgD1.
- Following this interaction, the signs of infection developed as clusters of rounded cells, and this infectivity was shown to continue when transferred to other RKgD1 cells.
Study Findings
- The progeny virus, resulting from this interaction, demonstrated the ability to infect single RK cells as well, implying that EHV-4 acquires EHV-1 gD from the complementing cell line, leading to its infectivity.
- The study observed no similar cellular infection when EHV-4 interacted with RK cells expressing EHV-1’s glycoprotein C.
- The findings suggest that gD homologues could be major determinants in identifying target host cells (host cell tropism).
Significance and Implications
- The study suggests a potential link between gD protein and the contrasting pathogenic abilities of EHV-1 and EHV-4, posing a new inquiry in understanding virus formation and propagation.
- Should future research confirm the implications of this study, it could enhance our understanding of the differential pathogenicity of EHV-1 and EHV-4 and possibly lead to specific antiviral targeting strategy.
Cite This Article
APA
Whalley JM, Ruitenberg KM, Sullivan K, Seshadri L, Hansen K, Birch D, Gilkerson JR, Wellington JE.
(2006).
Host cell tropism of equine herpesviruses: glycoprotein D of EHV-1 enables EHV-4 to infect a non-permissive cell line.
Arch Virol, 152(4), 717-725.
https://doi.org/10.1007/s00705-006-0885-x Publication
Researcher Affiliations
- Department of Chemistry and Biomolecular Sciences, Macquarie University, Sydney, Australia. mwhalley@rna.bio.mq.edu.au
MeSH Terms
- Animals
- Cell Line
- Herpesvirus 1, Equid / genetics
- Herpesvirus 4, Equid / physiology
- Microscopy, Confocal
- Rabbits
- Viral Envelope Proteins / biosynthesis
- Viral Envelope Proteins / genetics
- Viral Envelope Proteins / physiology
- Virus Internalization
Citations
This article has been cited 9 times.- Muscat KE, Padalino B, Hartley CA, Ficorilli N, Celi P, Knight P, Raidal S, Gilkerson JR, Muscatello G. Equine Transport and Changes in Equid Herpesvirus' Status.. Front Vet Sci 2018;5:224.
- Mori E, Lara Mdo C, Cunha EM, Villalobos EM, Mori CM, Soares RM, Brandu00e3o PE, Fernandes WR, Richtzenhain LJ. Molecular characterization of Brazilian equid herpesvirus type 1 strains based on neuropathogenicity markers.. Braz J Microbiol 2015 Jun;46(2):565-70.
- Spiesschaert B, Osterrieder N, Azab W. Comparative analysis of glycoprotein B (gB) of equine herpesvirus type 1 and type 4 (EHV-1 and EHV-4) in cellular tropism and cell-to-cell transmission.. Viruses 2015 Feb 3;7(2):522-42.
- Kong C, Zhao Y, Cui X, Zhang X, Cui H, Xue M, Wang Y. Complete genome sequence of the first Chinese virulent infectious laryngotracheitis virus.. PLoS One 2013;8(7):e70154.
- Azab W, Zajic L, Osterrieder N. The role of glycoprotein H of equine herpesviruses 1 and 4 (EHV-1 and EHV-4) in cellular host range and integrin binding.. Vet Res 2012 Aug 21;43(1):61.
- Azab W, Osterrieder N. Glycoproteins D of equine herpesvirus type 1 (EHV-1) and EHV-4 determine cellular tropism independently of integrins.. J Virol 2012 Feb;86(4):2031-44.
- Sasaki M, Kim E, Igarashi M, Ito K, Hasebe R, Fukushi H, Sawa H, Kimura T. Single amino acid residue in the A2 domain of major histocompatibility complex class I is involved in the efficiency of equine herpesvirus-1 entry.. J Biol Chem 2011 Nov 11;286(45):39370-8.
- Sasaki M, Hasebe R, Makino Y, Suzuki T, Fukushi H, Okamoto M, Matsuda K, Taniyama H, Sawa H, Kimura T. Equine major histocompatibility complex class I molecules act as entry receptors that bind to equine herpesvirus-1 glycoprotein D.. Genes Cells 2011 Apr;16(4):343-57.
- Ahn B, Zhang Y, Osterrieder N, O'Callaghan DJ. Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region.. Virology 2011 Feb 20;410(2):327-35.