Thus, the elevations in serum IFN-α levels observed in patients with early infection and advanced HIV disease [141], despite the diminished in vitro ability of pDCs to produce IFN-α following stimulation described above have been explained in the sense that IFN-I or even HIV virions may have activated pDCs previously, hindering their IFN-I production when they are later stimulated in vitro [141]. This evidence concerns the gene IFNA2 and infection.