We previously illustrated that DCs exposed to HIV-C elicit a significantly stronger type I IFN response via a CR4/CCR5/RLR (RIG-I/MDA5)/MAVS/TBK1/IRF3/NFκB signaling axis, and therefore, in co-cultures with CD4+ T cells, the lower level of productive infection despite higher TNT formation could be attributed to this higher type I IFN production and therefore a better antiviral response in HIV-C-infected DCs [18,19]. The gene discussed is IRF3; the disease is infection.