Abstract
An increase in the rate of isolation of Candida parapsilosis in the past decade, as well as increased identification of azole-resistant strains are concerning, and require better understanding of virulence-like factors and drug-resistant traits of these species. In this regard, the present review “draws a line” on the information acquired, thus far, on virulence determinants and molecular mechanisms of antifungal resistance in these opportunistic pathogens, mainly derived from genetic manipulation studies. This will provide better focus on where we stand in our understanding of the C. parapsilosis species complex–host interaction, and how far we are from defining potential novel targets or therapeutic strategies—key factors to pave the way for a more tailored management of fungal infections caused by these fungal pathogens.
Highlights
We witnessed an increase in the frequency of invasive fungal infections worldwide and a significant change in the epidemiological scenario: if Candida albicans dominated the clinical setting over the last century, non-albicans Candida (NAC) species are on the rise [1,2]
No genetic manipulation studies have been performed to date to dissect the role of this gene family in any of the members of the C. parapsilosis species complex. This would be of extreme interest in order to explain the apparent incongruence between the reduced pathogenicity of C. metapsilosis and its expansion of the IPF family F/hyphal-upregulated protein (IFF/HYR) gene family compared to C. orthopsilosis
CpCDR1 and CpMDR1 respectively, and the regulation of different proteins contributing to azole resistance was suggested. These results indicated that CpCDR1 and CpMDR1 overexpression partially contributes to the azole resistance in C. parapsilosis
Summary
We witnessed an increase in the frequency of invasive fungal infections worldwide and a significant change in the epidemiological scenario: if Candida albicans dominated the clinical setting over the last century, non-albicans Candida (NAC) species are on the rise [1,2]. Generation of null mutants is achieved by auxotrophic complementation obtained via the sequential targeting of each allele with a different nutritional marker This approach was used in C. parapsilosis for the construction of a large-scale gene deletion collection carrying mutations in 100 genes encoding for transcription factors, protein kinases, and species-specific proteins [50]. C. parapsilosis heterozygous strains were obtained either by varying the distance between the Cas DSB site and the inserted DNA or via transformation with two different repair templates Both the pRIBO plasmid approach and the tRNA strategy, were used for the efficient generation of mutant strains in the closely related species, C. orthopsilosis and C. metapsilosis [28,58] demonstrating, once again, the versatile applicability of genetic manipulation systems among members of the same complex. No effect in posaconazole resistance was observed [28]
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