The study demonstrates that human rhinovirus HRV14 uncoating is catalyzed by the viral receptor alone and can occur from early endocytic compartments without endosomal acidification.
Determination of infectious progeny virus and in vivo labelling with (35)Smethionine followed by immunoprecipitation demonstrates that the major receptor group human rhinovirus HRV14 is able to infect HeLa cells in the presence of the V-ATPase inhibitor bafilomycin A1. However, host cell shut off is delayed and viral yield is decreased in the presence of the drug. Uncoating can thus take place under conditions that prevent endosomal acidification indicating that it is catalysed by the viral receptor alone. Since transport is arrested in early endosomes upon inhibition of vesicle acidification, the data also suggest that productive uncoating takes place from early endocytic compartments.
Bayer et al. (Tue,) studied this question.
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