Essaidi–Laziosi M et al. – This study compared infections caused by respiratory viruses that are isolated from clinical specimens using reconstituted human airway epithelia. Results of the study highlighted differential in vitro pathogenesis of respiratory viruses during the acute infection phase and their ability to survive under immune tolerance. These observations help in understanding the spectrum of the disease severity observed in vivo and the occurrence of chronic respiratory infections in immunocompromised hosts.

Methods

• Comparison of replication kinetics, cell tropism, effect on tissue integrity, and cytokine secretion were performed following infection of tissues with rhinoviruses (RV–A55, RV–A49, RV–B48, RV–C8, and RV–C15), respiratory enterovirus (EV–D68), influenza virus (H3N2), respiratory syncytial virus (RSV–B), and coronavirus (HCoV–OC43).
• Viral adaptation and tissue response were assessed by ribonucleic acid (RNA) sequencing.

Results

• No major cell death was caused by infection of ciliated cells with rhinoviruses ,RSV–B and HCoV–OC43; however, ciliated cell loss and tissue integrity disruption were induced by H3N2 and EV–D68.
• H3N2 detected in rare goblet and basal cells was the strongest cytokine inducer, whereas HCoV–OC43 was the weakest cytokine inducer.
• Cilia beating and mucociliary clearance were altered by all the viruses, except RV–B48 and HCoV–OC43.
• Persistent infection was observed in all cases. No majority mutations were reported in the viral population.
• Perturbation of tissue metabolism and induction of a temporary but vital immune response 4 days post–infection were observed (RNA sequencing).