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.

• Authors: J M Whalley, K M Ruitenberg, K Sullivan, L Seshadri, K Hansen, D Birch, J R Gilkerson, J E Wellington
• Journal: Archives of virology (Arch Virol) Vol. 152 Issue 4 Pg. 717-25 ( 2007) ISSN: 0304-8608 [Print] Austria
• PMID: 17171298 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Viral Envelope Proteins
• glycoprotein C, Equid herpesvirus 1
• glycoprotein D, Equid herpesvirus 1

Topics

• Animals
• Cell Line
• Herpesvirus 1, Equid (genetics)
• Herpesvirus 4, Equid (physiology)
• Microscopy, Confocal
• Rabbits
• Viral Envelope Proteins (biosynthesis, genetics, physiology)
• Virus Internalization