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Virulence studies were performed using the murine inhalation model.
The murine inhalation model of systemic Cryptococcosis was performed as described before [66].
However, the pmt1 and pmt4 mutants showed attenuated virulence in a murine inhalation model of cryptococcosis.
Overall virulence of C. neoformans strains was tested by macrophage killing assays and by a murine inhalation model.
In this study, we demonstrate that C. gattii requires calcineurin (Cna1) for thermotolerance and virulence in a murine inhalation model.
In the murine inhalation model, we initially observed apparently similar virulence between strains F2 and H99, whereas F0 appeared attenuated.
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In the murine inhalation infection model, the met3 mutant was avirulent and was deficient in its ability to survive in mice [ 71].
The C. neoformans ilv2∆ mutant was unable to survive in vivo in the murine nasal inhalation model (Pascon et al. 2004).
In addition, the C. neoformans met3∆ mutant is avirulent in the murine intranasal inhalation model (Kwon-Chung et al. 1982; Kwon-Chung and Rhodes 1986; Rhodes et al. 1982) and the production of melanin, a known virulence factor, is depleted (Yang et al. 2002).
In summary, our data suggest that in C. gattii calcineurin promotes thermotolerance and other mechanisms during infection in both the murine inhalation and wax moth models, in addition to a requirement for calcineurin in azole tolerance of C. gattii.
We demonstrated that C. gattii R265, R272, and WM276 wild-type strains exhibited similar virulence between murine inhalation and wax moth infection models.
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