CCL5 is activated as a pro-inflammatory chemokine during primary respiratory syncytial virus (RSV) infection.[53] During influenza infection in airway and lung cells, IFIT3 can limit the spread of virus, affect the severity of infection and improve cellular defense against virus, IFIT3 may be an important mediator of influenza antiviral response.[54] Therefore, it is speculated that SPI1 is involved in and amplifies the inflammatory response in the progression of COVID-19. This evidence concerns the gene CCL5 and COVID-19.