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Fig. 5.
Entry pathways of major and minor group HRVs in HeLa cells,
exemplified by HRV14 and HRV2. HRV14 is internalized via clathrin-
coated pits and vesicles (CCV) and delivered into early endosomes, where
the receptor-catalyzed conformational change can take place at 34
C.
Presumably, the structural modification is coupled to RNA release and rup-
ture of the endosomal membrane resulting in delivery of free RNA and
empty capsids into the cytoplasm. Consequently, the majority of virus escapes
further transport to lysosomes. At least HRV3 and HRV14 can uncoat at
neutral endosomal pH in the presence of bafilomycin and thus in early
endosomes. HRV2 enters via clathrin-dependent and independent pathways
and dissociates from its receptors at mildly acidic pH in early endosomes.
Receptors are recycled and HRV2 is transferred to endosomal carrier vesi-
cles (ECV), where the more acidic pH (
°
5.6) induces the structural mod-
ification, resulting in RNA uncoating and transfer into the cytosol. Note
that ECV and late endosomes are multivesicular bodies and thus contain
many internal vesicles. Presumably, the RNA can also be translocated into
the internal vesicles of ECV. Finally, residual native virus, subviral particles
and viral RNA are transported via late endosomes to lysosomes, where they
are degraded.
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