Canine herpesvirus 1 (CHV-1) has a relatively narrow host cell range when c
ompared to other alphaherpesviruses. The early events of CHV-1 infection in
a permissive Madin-Darby canine kidney (MDCK) and non-permissive cell line
s. In order to quantify attachment and penetration, were investigated quant
itative competitive PCR (QCPCR) method was established for quantitation of
CHV-1 DNA. In all non-permissive cells tested, no significant decrease in v
iral attachment was observed. When CHV-1 was treated with heparin, viral at
tachment to MDCK cells was reduced by 25% of the input CHV-1 attached to MD
CK cells even in the presence of 50 mu g /ml heparin. However, the attachme
nt of CHV-1 to non-permissive cells was severely impaired by heparin treatm
ent. In permissive MDCK cells, about 80% of attached CHV-1 penetrated into
cells. However, only 4-10 % of CHV-1 attached to non-permissive cells penet
rated into cells. Our data indicated that CHV-1, like other herpesviruses,
attached to permissive MDCK cells through two mechanisms: the first one is
through the interaction mediated by heparan sulfate (HS) on the cell surfac
e and the second involves unidentified viral component and the cellular rec
eptor. In contrast, the non-permissive cells lacked the cellular receptor f
or the second attachment mechanism and the defect in viral penetration into
non-permissive cell might be related to the lack of the cellular receptor.