For example, exposure of macrophages to continuous low levels of IFN-α leads to enhanced IFN-γ induction of interleukin (IL)-12p70 through favoured STAT1 homodimer formation, in contrast to exposure to high levels of type I IFN, which inhibits IFN-γ-induced activation of major histocompatibility complex (MHC) class II expression and dampens IL-12p70 production.12 Thus, virus infections induce immune responses by eliciting production of type I IFNs, which in turn exert effects that include sustained clonal expansion, differentiation and survival of proliferating cells. This evidence concerns the gene IFNA1 and viral infectious disease.