INTRACELLULAR ROUTE OF CANINE PARVOVIRUS ENTRY

The present study was designed to investigate the endocytic pathway in volved in canine parvovirus (CPV) infection. Reduced temperature (18 d egrees C) or the microtubule-depolymerizing drug nocodazole was found to inhibit productive infection of canine A72 cells by CPV and caused CPV to be retained in cytoplasmic vesicles as indicated by immunofluor escence microscopy. Consistent with previously published results, thes e data indicate that CPV enters a host cell via an endocytic route and further suggest that microtubule-dependent delivery of CPV to late en dosomes is required for productive infection. Cytoplasmic microinjecti on of CPV particles was used to circumvent the endocytosis and membran e fusion steps in the entry process. Microinjection experiments showed that CPV particles which were injected directly into the cytoplasm, t hus avoiding the endocytic pathway, were unable to initiate progeny vi rus production. CPV treated at pH 5.0 prior to microinjection was unab le to initiate virus production, showing that factors of the endocytic route other than low pH are necessary for the initiation of infection by CPV.