Individuals with Down syndrome have fewer viral infections, but when infected, they suffer from more severe disease. Malle et al. find that triplication of IFNAR1 and IFNAR2, the receptor subunits of the potent antiviral cytokine IFN-I, in DS results in hyperactive IFN-I signaling. The ensuing hyperinduction of IFNAR negative regulators suppresses subsequent IFN-I stimuli and effectively represses further antiviral defenses.
Source: Malle et al.