KIR2DL3 and viral infectious disease: KIR2DL3 with HLA-C1 is considered a weaker interaction than KIR2DL1 with HLA-C2, allowing disease associations to be explained through the “strength of inhibition” hypothesis, with weaker inhibitory receptor interactions leading to more NK cell activation and clearance of viral infections such as HCV (3, 6, 7, 12–15).