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. 2004 Jul;78(13):7186–7198. doi: 10.1128/JVI.78.13.7186-7198.2004

FIG. 10.

FIG. 10.

Hypothesis for mechanisms of early infection of PV. (A) PV interacts with hPVR and fuses with the lipid bilayer on the cellular membrane, and then the viral genomic RNA transfers into the cytoplasm. This is mainly observed in HeLa cells (8). (B) PV adheres to hPVR and is incorporated into endosomes. The pH or other factors inside the endosomes might make PV unstable and cause the release of its genomic RNA into the cytoplasm. This is also observed in HeLa cells (43). (C) PV adheres to hPVR and is incorporated into endosomes. The endosomes are transported by dynein along microtubules, and the viral genomic RNA transfers into the cytoplasm. PV fuses with the lipid bilayer on the endosomal membrane under particular conditions. This possibly occurs in HeLa cells, as well as neural cells.