Following viral infection, the expression of substance P and its receptor can contribute significantly to the resulting host response. For gammaherpesvirus infection of mice, the presence of this tachykinin and its receptor contributes to the protective host response. It is likely that this augmentation of the immune response is directed toward the developing T helper type 1 response and cytotoxic T lymphocyte activation. However it has also been shown that the presence of substance P and its receptor may contribute to viral diseases by facilitating viral replication or by contributing to a destructive inflammatory response. Specifically, the presence of substance P can augment replication of HIV in cultured macrophages, which is especially significant since levels of this tachykinin are elevated in patients with this viral disease. Furthermore, rodent models of paramyxovirus infection have demonstrated that the presence of neurokinin receptors and their ligands contributes to the destructive inflammatory response in airways. Taken together, these studies demonstrate a surprising role for substance P and the neurokinin-1 receptor in the host response following these viral infections.