The murine inhalation model inoculated with a strain of Cryptococcus neoformans lacking Mpr1 showed significant improvement in survival due to a lack of.

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The murine inhalation model inoculated with a strain of Cryptococcus neoformans lacking Mpr1 showed significant improvement in survival due to a lack of fungal burden in the brain. The murine inhalation model inoculated with a strain of Cryptococcus neoformans lacking Mpr1 showed significant improvement in survival due to a lack of fungal burden in the brain. (A) Shown is percent survival of mice inoculated via the nares, mimicking the natural route of infection, with the H99 (wild type), mpr1Δ, and MPR1 (mpr1Δ::MPR1; reconstituted strain) strains. Mpr1Δ strain-infected mice showed a significant improvement in survival (P = 0.001, Wilcoxon test, sample size determined by power analysis [GPower3.1]) (B and C) CFUs representing the fungal burden at the time of death in lungs (B) or brains (C) of mice inoculated with H99, the mpr1Δ mutant, and the MPR1-reconstituted strains revealed significantly less fungal burden in brains from mice infected with the mpr1Δ mutant strain (**, P = 0.009). (D) Following 10 days p.i. (postinfection), mpr1Δ strain-infected mice and H99-infected mice showed similar fungal burdens in lungs, kidneys, spleen, and heart, suggesting that Mpr1 is not required for dissemination out of the lung and Mpr1 does not play a role in breaching other vascular endothelia (P > 0.05 for all tissues). Kiem Vu et al. mBio 2014; doi:10.1128/mBio.01101-14