UV light inhibited HRV1b replication but reduced adherent epithelial junction and antiviral responses via SOCS1 in human respiratory epithelial cells
Authors: Finotto Susetta , Maimuna Jeba , Yang Zuqin , Bachmann Elke , Susanne Mittler , Trump Sonja 
Published: October 2024

Asthma is a chronic respiratory disorder characterized by the pathologic recruitment and activation of inflammatory cells in the bronchioles. This results in bronchial hyperreactivity, recurrent breathlessness, and wheezing. Rhinovirus (RV) is one of the common respiratory viral infections that triggers airway obstruction and exacerbations, especially during childhood. To limit airborne viral transmission, inactivating the virus reproduction for a short time can be an option. Light technologies like Ultraviolet (UV) and Infrared (IF) radiations have antimicrobial properties, however the timing and mechanism of action are not known. This project aimed at evaluating the mechanism of Ultraviolet (UV) and Infrared (IR) radiations to inactivate RV inside and outside infected cells and the resulting impact on Interferon responses and epithelial barrier integrity.
Specifically, the A549 cell line (human adenocarcinoma alveolar basal epithelial cell line), as well as the cell culture of Nasal Epithelial Cells (NEC) differentiated from the Nasal Pharyngeal fluid were used because the airway epithelial cells are the primary site of human rhinovirus (HRV) infection and replication in both the upper and lower airways in human. Hereby these airway epithelial cells were infected with different RV concentrations and analyzed at different time points to evaluate the amount of intracellular and extracellular RV mRNA by qPCR. Later, these airway epithelial cells were exposed to different lights particularly UV and IR to analyze the impact on the viral immune response of the host. At the end of the cell culture, anti-viral (INF-l & INF-ll) and tight junction components were measured by real-time PCR.
It was found that RV1B disrupted cell junctions of airway epithelial cell barriers and changed the epithelial cell membrane permeability which can potentially induce the risk of asthma. It was also seen that high doses of RV1B activated pattern recognition receptor (TLR3), induced interferon (IFNβ) response and reduced SOCS1, which is a negative regulator of IFNβ. Therefore, to inactivate the RV1B, we have been targeting two germicidal light technologies, UVC and IR. Here, we examined the change related to RV1B inactivation, epithelial barrier integrity, and interferon response in epithelial cells after UVC and IR irradiation.
Firstly, IR irradiation was used to examine whether and to what extent the light can destroy RV in epithelial cells and alter epithelial barrier integrity and interferon response. It was noticed that IR lights do not have the ability to inhibit rhinovirus. Nevertheless, IR treatment shows low antiviral function. Therefore, we analyzed UVC light to check the ability of epithelial barrier integrity and interferon response in airway epithelial cells. Our findings suggested that UVC exposure significantly decreased RV1B within 72h. Moreover, RV1B induced the antiviral pathways in the host cells via inducing TLR3 expression and IFN-beta response whereas UV 72h treatment inhibited the antiviral effects of the host via SOCS1. Collectively, these findings support the role of UV 72h treatment as an effective therapeutic approach for acutely eliminating the RV but resulting in a barrier and antiviral damage which can have a drawback effect in asthmatics.
These studies should lead to a better understanding of the effect of the germicidal light on RV on the epithelial barrier and its integrity and its antiviral function. Moreover, these studies can lead to establishing better therapeutic interventions with fewer side effects for asthmatic patients.