Fig. 1. AHR is a candidate therapeutic target for viral infection.

AHR activation during viral infection results in the upregulation of IDO/TDO, which convert tryptophan to Kynurenine (Kyn). Kyn activates AHR, leading to formation of an AHR–ligand complex that limits host anti-viral responses mediated by IFN-I and NF-κB, thus promoting viral replication. AHR signaling also induces mucin expression in lung epithelial cells, thickening the blood–air barrier, impairing O₂ diffusion and causing hypoxia. AHR antagonists limit AHR activation, boosting the host anti-viral response and consequently reducing viral replication. AHR antagonism also reduces the expression of mucins, limiting lung pathology during SARS-CoV-2 infection.