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Cryptococcus neoformans andCryptococcus gattii cause fatal infection in immunodeficient and immunocompetent individuals. While these fungi are sibling species,C. gattii infects very few AIDS patients, whileC. neoformans infection is an AIDS-defining illness, suggesting that the host response to HIV selectsC. neoformans overC. gattii . We used a viral mimic molecule (pICLC) to stimulate the immune response, and pICLC treatment improved mouse outcomes from both species. pICLC-induced action againstC. neoformans was due to activation of well-defined immune pathways known to deterC. neoformans , whereas these immune pathways were dispensable for pICLC treatment ofC. gattii . Since these immune pathways are eventually destroyed by HIV/AIDS, our data help explain why the antiviral immune response in AIDS patients is unable to controlC. neoformans infection but is protective againstC. gattii . Furthermore, pICLC induced tighter control of iron in the lungs of mice, which inhibitedC. gattii , thus suggesting an entirely new mode of nutritional immunity activated by viral signals.

Pulmonary Iron Limitation Induced by Exogenous Type I IFN Protects Mice from Cryptococcus gattii Independently of T Cells