PRDI and III are binding sites for IRF3 (early during infection, due to its constitutive expression) and IRF7 (with delayed kinetics, due to its inducible expression through an IFN-dependent positive feedback loop), while PRDIV and PRDII bind the ATF-2/c-Jun AP-1 and the p50/RelA NF-κB complexes respectively (reviewed in [8]). The gene discussed is ATF2; the disease is infection.