Entry of poliovirus type 1 and Mouse Elberfeld (ME) virus into HEp-2 cells: receptor-mediated endocytosis and endosomal or lysosomal uncoating.
Poliovirus type 1 appeared from electron microscope studies to enter HEp-2 cells by receptor-mediated endocytosis. On adsorption the virus was evenly distributed over the cell surface, with some preference for the microvilli and their bases. Invagination of the cell surface membrane with the attached virus commenced at coated pits and led to the formation of virus-containing coated vesicles in the cytoplasm. These coated vesicles fused with intracellular vesicles to form endosomes. When cells infected with poliovirus or Mouse Elberfeld virus were treated with the weak bases chloroquine, NH4Cl or the ionophore monensin to raise the intraendosomal and intralysosomal pH above 6, virus-directed macromolecular synthesis and production of progeny were prevented. These results suggest that the virus genomes are released to the cytoplasm via endosomes and/or lysosomes by a pH-dependent process.
Zeichhardt
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Wetz
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Willingmann
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Habermehl
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D000643:Ammonium Chloride / Q000494:pharmacology; D002460:Cell Line; D002738:Chloroquine / Q000494:pharmacology; D004705:Endocytosis; D011992:Endosomes / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D008247:Lysosomes / Q000502:physiology*; D008985:Monensin / Q000494:pharmacology; D010849:Picornaviridae / Q000254:growth & development*; D017955:Poliovirus / Q000254:growth & development*; D012367:RNA, Viral / Q000096:biosynthesis; D014779:Virus Replication
D012367:RNA, Viral; D000643:Ammonium Chloride; D002738:Chloroquine; D008985:Monensin