Abstract
Canine herpesvirus 1(CHV−1)has a relatively narrow host cell range when compared to other alphaherpesviruses.The early events of CHV−1 infection in a permissive Madin−Darby canine kidney(MDCK)and non−permissive cell lines.In order to quantify attachment and penetration, were investigated quantitative competitive PCR(QCPCR)method was established for quantitation of CHV−1 DNA.In all non−permissive cells tested, no significant decrease in viral attachment was observed.When CHV−1 was treated with heparin, viral attachment to MDCK cells was reduced by 25% of the input CHV−1 attached to MDCK cells even in the presence of 50 μg/ml heparin.However, the attachment of CHV−1 to non−permissive cells was severely impaired by heparin treatment.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 penetrated 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 surface and the second involves unidentified viral component and the cellular receptor.In contrast, the non−permissive cells lacked the cellular receptor for the second attachment mechanism and the defect in viral penetration into non−permissive cell might be related to the lack of the cellular receptor.
