Using this model, modulation of receptor expression, as well as increases in β-chemokines or IFNα production have been proposed, among others, as mechanisms that contribute to the reduced HIV-1 infection in LPS-stimulated MDMs [12]–[18], while no clear mechanism has been reported for poly(I∶C)-induced restriction of HIV-1 infection in MDMs [22]–[24]. The gene discussed is IFNA1; the disease is HIV-1 infection.