# UV Light Inhibited HRV1b Replication but Reduced Adherens Epithelial Junction and Antiviral Responses via SOCS1 in Human Respiratory Epithelial Cells

## TL;DR

UV light can reduce HRV replication but may also weaken airway defenses and epithelial barriers, potentially worsening asthma.

## Contribution

Demonstrates UV light's dual effect on HRV inhibition and epithelial junction/antiviral response disruption via SOCS1.

## Key findings

- UVC exposure significantly inhibited HRV1b replication within 72 hours.
- UV light reduced SOCS1, weakening antiviral responses and epithelial junction integrity.
- IR light inhibited HRV post-infection in nasal epithelial cells.

## Abstract

Human rhinovirus (HRV) is one of the common respiratory viral infection agents that triggers airway obstruction and asthma exacerbations, especially during childhood. This project aimed at evaluating the mechanism of ultraviolet (UV) and infrared (IR) radiations to inactivate HRV infection and replication inside and outside infected airway epithelial cells and the resulting impact on interferon responses and epithelial barrier integrity. Hereby, airway epithelial cells were infected with different RV concentrations. Later these cells are exposed to UV and IR light to analyze their impact on the viral immune response of the host by real-time PCR. It was found that RV1B disrupted cell junctions of airway epithelial cell barriers. Moreover, high doses of RV1B activated pattern recognition receptor (TLR3), induced interferon (IFN-β) response and reduced SOCS1, which is a negative regulator of IFN-β. Further, IR lights inhibited rhinovirus post infection in primary nasal epithelial cells (NECs). Finally, UVC exposure significantly inhibited the antiviral effects of the host via SOCS1 inhibition and decreased RV1B within 72 h. Collectively, these findings support the role of UV light as an effective therapeutic approach for acutely eliminating RV but resulting in barrier and antiviral damage, which can have a drawback effect for asthma.