Publications by authors named "Sophie Altamirano"

Cryptococcus neoformans, a basidiomycete yeast, causes lethal meningitis in immunocompromised individuals. The ability of C. neoformans to proliferate at 37°C is essential for virulence.

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The pathogenic yeast Cryptococcus neoformans produces polyploid titan cells in response to the host lung environment that are critical for host adaptation and subsequent disease. We analyzed the and cell cycles to identify key aspects of the C. neoformans cell cycle that are important for the formation of titan cells.

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Fungal hyphal growth and branching are essential traits that allow fungi to spread and proliferate in many environments. This sustained growth is essential for a myriad of applications in health, agriculture, and industry. However, comparisons between different fungi are difficult in the absence of standardized metrics.

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As the existing therapeutic modalities for the treatment of cryptococcal meningitis (CM) have suboptimal efficacy, repurposing existing drugs for the treatment of CM is of great interest. The FDA-approved anthelmintic benzimidazoles, albendazole, mebendazole, and flubendazole, have demonstrated potent but variable activity against , the predominant fungal species responsible for CM. We performed molecular docking studies to ascertain the interaction of albendazole, mebendazole, and flubendazole with a β-tubulin structure, which revealed differential binding interactions and explained the different efficacies reported previously and observed in this investigation.

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Half maximal inhibitory concentrations (IC) to the experimental drug ATI-2307 and complete inhibition (IC) of the common clinically used antifungal drug amphotericin B were determined by microbroth dilution assay for a collection of 69 clinical isolates of from Uganda that had high fluconazole IC values. The majority of the clinical isolates tested had fluconazole IC at or above 8 µg/mL, but were susceptible to both amphotericin B (IC ≤1 μg/mL) and ATI-2307 (IC50 ≤0.0312 µg/mL).

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Cryptococcus neoformans is an opportunistic fungal pathogen that causes life-threatening meningitis primarily in immunocompromised individuals. In order to survive and proliferate during infection, C. neoformans must adapt to a variety of stresses it encounters within the host.

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Increasing resistance to frontline antifungals is a growing threat to global health. In the face of high rates of relapse for patients with cryptococcal meningitis and frequent drug resistance in clinical isolates, recent insights into Cryptococcus neoformans morphogenesis and genome plasticity take on new and urgent meaning. Here we review the state of the understanding of mechanisms of drug resistance in the context of host-relevant changes in Cryptococcus morphology and cell ploidy.

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is a human fungal pathogen that can cause fatal meningitis in immunocompromised individuals. Fluconazole (FLC) is a fungistatic drug administered to treat cryptococcosis. When exposed to the inhibitory concentration of FLC, exhibits heteroresistance where a small subpopulation of cells develops into FLC-resistant colonies.

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While mechanisms of cytokinesis exhibit considerable plasticity, it is difficult to precisely define the level of conservation of this essential part of cell division in fungi, as majority of our knowledge is based on ascomycetous yeasts. However, in the last decade more details have been uncovered regarding cytokinesis in the second largest fungal phylum, basidiomycetes, specifically in two yeasts, and . Based on these findings, and current sequenced genomes, we summarize cytokinesis in basidiomycetous yeasts, indicating features that may be unique to this phylum, species-specific characteristics, as well as mechanisms that may be common to all eukaryotes.

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is a pathogenic yeast that causes lethal cryptococcal meningitis in immunocompromised patients. One of the challenges in treating cryptococcosis is the development of resistance to azole antifungals. Previous studies linked azole resistance to elevated numbers of copies of critical resistance genes in aneuploid cells.

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