Infection with either HCMV strain significantly suppressed numerous pathways associated with immune recognition of fungal antigens (e.g., Toll-like receptor signaling), inflammasome and acute phase response signaling, key antifungal effector cytokine responses (e.g., IFN-γ, IL-6, IL-8, and IL-17 signaling), activation and maturation of mononuclear phagocytes, and intercellular communication during co-infection (Fig. 6A). Here, IL17A is linked to infection.