TY - JOUR
T1 - Host cell tropism of equine herpesviruses
T2 - Glycoprotein D of EHV-1 enables EHV-4 to infect a non-permissive cell line
AU - Whalley, J. M.
AU - Ruitenberg, K. M.
AU - Sullivan, K.
AU - Seshadri, L.
AU - Hansen, K.
AU - Birch, D.
AU - Gilkerson, J. R.
AU - Wellington, J. E.
PY - 2007/4
Y1 - 2007/4
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33947427940&partnerID=8YFLogxK
U2 - 10.1007/s00705-006-0885-x
DO - 10.1007/s00705-006-0885-x
M3 - Article
C2 - 17171298
AN - SCOPUS:33947427940
SN - 0304-8608
VL - 152
SP - 717
EP - 725
JO - Archives of Virology
JF - Archives of Virology
IS - 4
ER -