1. HaCaT epithelial cells as an innovative novel model of rhinovirus infection and impact of clarithromycin treatment on infection kinetics.
- Author
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Morgene MF, Maurin C, Pillet S, Berthelot P, Morfin F, Pozzetto B, Botelho-Nevers E, and Verhoeven PO
- Subjects
- Cell Line, Transformed, Cell Survival drug effects, Gene Expression drug effects, Genotype, Humans, Intercellular Adhesion Molecule-1 metabolism, Keratinocytes drug effects, Keratinocytes metabolism, Keratinocytes virology, Receptors, Virus antagonists & inhibitors, Receptors, Virus metabolism, Rhinovirus classification, Rhinovirus growth & development, Rhinovirus metabolism, Viral Load drug effects, Virion drug effects, Virion growth & development, Virion metabolism, Virus Replication drug effects, Clarithromycin pharmacology, Host-Pathogen Interactions drug effects, Intercellular Adhesion Molecule-1 genetics, Protein Synthesis Inhibitors pharmacology, Receptors, Virus genetics, Rhinovirus drug effects
- Abstract
The in vitro propagation of human rhinoviruses (RVs) is difficult because only few continuous human cell lines are permissive to these agents. We propose an innovative model of epithelial cell infection using a non-transformed continuous keratinocyte line from human origin (HaCaT cells). After infection with RV-A13, RV-A16 or RV-A19, HaCaT cells produced infectious particles without showing any observable cytopathic effect and overexpressed ICAM-1 (intercellular adhesion molecule 1), the major entry receptor of RVs. Furthermore, the treatment of HaCaT cells with 10 µM clarithromycin reduced the viral titer by 93% and 60% during the first and second days following viral infection, respectively, probably by down-regulating ICAM-1 expression. This original model of epithelial cell infection by RV could be useful to study chronic viral infection and bacterium-virus interactions at the cell level. These results also suggest that clarithromycin may be evaluated for treating in vivo infections associating RV to a susceptible bacterium., (Copyright © 2018. Published by Elsevier Inc.)
- Published
- 2018
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