The Subcellular Localization and the Tissue Tropism of Canine Parvovirus based on the Co-localization of Transferrin Receptors
Canine parvovirus type 2 (CPV-2) has emerged as a pathogen of new acute infectious disease in dogs. It affects primarily young animals where it can cause haemorrhagic enteritis and myocarditis. Receptor binding is a key step in the life cycles of all animal viruses. It has been reported that the specific binding to transferrin receptor (TfR) on cell membranes plays an important role in tissue tropism and host ranges of CPV-2. In this study, the entry and the subcellular localization of viral particles and TfR in the cells of FK81 and MDCK were analyzed; the distribution of TfR and infectious ability of CPV-2 were determined in the cells of various primary tissue cultures from dog fetus. We observed complicated temporal patterns of CPV-2 virus particle trafficking during post-incubation with cells of FK81 and MDCK. The virus particles were located in the cytoplasm 4-8 h after inoculation, they appeared in nuclei at 12-16 h of post-incubation, then reappeared in cytoplasm at 24 h again; they distributed all over the cellular organelles after 32 h incubation. The virus and the transferrin were co-located in the perinuclear cytoplasm after 2 h of incubation with the FK81 cells; addition of excessive transferrin decreased the rate of infection of CPV-2, but did not block virus entry. We found that CPV-2 replicated in primary culture cells of the liver, kidney, cardiac muscle, spleen and intestinal epithelia but not of the lung and internalization of transferrin receptor in primary cells was related to the culture tropism of CPV-2. These results confirmed that the TfR is critical for CPV-2 infection with both cell lines and primary tissue cells from fetes.
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