Experimental data show that increased susceptibility to influenza infection in COPD occurs through reduced induction of protein kinase R, an IFN-stimulated gene that is directly involved in limiting viral replications and in inducing IFN-γ through the binding of the recognition receptor, retinoic-acid inducible gene (RIG)I, to the adaptor mitochondrial signaling (MAVS) on the mitochondria. Here, IFNG is linked to chronic obstructive pulmonary disease.