Viruses cannot replicate by themselves. Instead, they rely on the host for almost all their replicative functions. Similarly, many viruses are unable to cause damage without the host immune system. Because of this, two strategies can often ameliorate disease — antivirals, which block replication, and antiinflammatories, which can limit the damage induced by infection. In the lung, this latter strategy is exemplified by the treatment of Pneumocystis jiroveci, in which treatment with glucocorticoids reduces the severity of disease and the risk of death.^1,2 However, because blocking inflammatory pathways raises the possibility of diminishing the host response and increasing replication of . . .