KIR3DL1 and viral infectious disease: This observation builds on prior work that identified an innate partnership between HLA-Bw4 molecules and high inhibitory KIR3DL1 subtypes (such as KIR3DL1∗001) in slowing HIV progression,30 given that strong inhibitory KIR3DL1 capacity is critical for NK cell development to quench autoreactivity49,50 and is subsequently associated with greater NK cell responsiveness during viral infections.51