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Our study reveals that respiratory syncytial virus (RSV) downregulates the aryl hydrocarbon receptor (AHR) pathway in human airway epithelial cells and mouse lungs. Loss of the AHR in lung cells led to an exacerbated inflammatory response, and the AHR ligand indole-3-carbinol (I3C) showed in vivo anti-inflammatory and antiviral activity during RSV infection. Our data suggest that AHR plays a protective role during RSV infection and can be explored as a novel therapeutic target.
Mello et al. (Wed,) studied this question.