Abstract
About 150 human rhinovirus serotypes are responsible for more than 50 % of recurrent upper respiratory infections. Despite having similar 3D structures, some bind members of the low-density lipoprotein receptor family, some ICAM-1, and some use CDHR3 for host cell infection. This is also reflected in the pathways exploited for cellular entry. We found that even rhinovirus serotypes binding the same receptor can travel along different endocytic pathways and release their RNA genome into the cytosol at different locations. How this may account for distinct immune responses elicited by various rhinoviruses and the observed symptoms of the common cold is briefly discussed.
Highlights
Human rhinoviruses (HRVs) account for more than 50 % of upper respiratory tract infections
How could the entry pathway taken by a given rhinovirus impact on the immune response? We presented evidence for HRV-A2 transferring its genome into the cytosol via a pore in the membrane and the remaining empty capsid being directed towards lysosomes where it is degraded
HRVs enter from the apical side of the cells lining the airways by receptor-mediated endocytosis via low-density lipoprotein receptor (LDLR) and ICAM-1
Summary
Human rhinoviruses (HRVs) account for more than 50 % of upper respiratory tract infections. * Correspondence: renate.fuchs@meduniwien.ac.at 1Department of Pathophysiology and Allergy Research, Medical University of Vienna, Währinger Gürtel 18-20, 1090 The cognate receptor must be accessible to the virus, i.e., at the apical surface of ciliated epithelial cells. Reinvestigating this issue, we detected ICAM-1 at the ciliated surface of all nasal epithelial cells in the nasal tissue from healthy individuals (Ellinger et al, to be published).
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