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Review
. 2004 Jul;78(13):6709-14.
doi: 10.1128/JVI.78.13.6709-6714.2004.

Pathways of cell infection by parvoviruses and adeno-associated viruses

Affiliations
Review

Pathways of cell infection by parvoviruses and adeno-associated viruses

Maija Vihinen-Ranta et al. J Virol. 2004 Jul.
No abstract available

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Figures

FIG. 1.
FIG. 1.
A schematic representation of the entry mechanisms utilized by parvoviruses within the host cell. Cell entry of autonomous parvovirus CPV and AAV is shown. After binding to their cell surface receptors, both viruses are internalized into clathrin-coated vesicles (CV), followed by transport to early (EE), late (LE), or perinuclear recycling endosomes (PNRE). Later in entry, in the case of AAV, capsids are found in Golgi compartments, whereas CPV can be found in lysosomes (LY). The site of the capsid escape from endocytic vesicles into the cytosol is still unclear. CPVs make use of microtubules (MT) during the traffic through the cytosol toward the nucleus. Viral capsids are able to enter the nucleus in intact form without apparent deformation.
FIG. 2.
FIG. 2.
Intracellular trafficking and modifications of autonomous parvovirus capsids. Once inside the cell, capsids undergo modifications, exposing on their surfaces not only the N-terminal end of the VP1 capsid protein but also the N-terminal sequence of the VP2 capsid protein and 3′ end of the viral genome. In the cytosol, capsids are also affected by the activity of proteasomes, possibly causing the intracellular formation of the VP3 capsid protein. Later in entry, viral capsids are imported into the nucleus through the NPC with the help of the NLS. MT, microtubules.

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