IFNG and viral infectious disease: This is supported by the fact that the HIV protease inhibitor ritonavir has been suggested to function, in part, by inducing HO-1.18 However, inhibition of HO-1 in cytomegalovirus-pp65-pulsed peripheral mononuclear cells resulted in increased antiviral T-cell activation and the generation of a higher proportion of memory T cells (CD45RA−CD62L−) capable of secreting IFN-γ and granzyme B.19 Thus, these findings suggest that the effect of HO-1 on viral infection is dependent on the particular viral etiology.