A recent study demonstrated that infection of human epithelial cells with a mutant RSV CX4C virus induced higher levels of interferon type I/III and TNF-α than a wild type CX3C virus, and the level of these cytokines was similar to the level induced by treatment of RSV-infected cells with mAb 131-2G, suggesting that the CX4C mutation reduces binding to CX3CR1 [34]. This evidence concerns the gene CX3CR1 and infection.