Our results suggest that TLR10 could mediate the extent of SARS-CoV-2 infection by downregulating the release of inflammatory cytokines and chemokines such as CXCL10, IL6, IL8, and IFNβ. Modulation of TLR10 expression could have implications for the treatment of patients with severe COVID-19, in whom excessive inflammation leading to the development of acute respiratory distress syndrome (ARDS) is a key feature. Here, IFNB1 is linked to acute respiratory distress syndrome.