Abstract
In order to successfully infect or colonize human hosts or survive changing environments, Aspergillus fumigatus needs to adapt through genetic changes or phenotypic plasticity. The genomic changes are based on the capacity of the fungus to produce genetic variation, followed by selection of the genotypes that are most fit to the new environment. Much scientific work has focused on the metabolic plasticity, biofilm formation or the particular genetic changes themselves leading to adaptation, such as antifungal resistance in the host. Recent scientific work has shown advances made in understanding the natural relevance of parasex and how both the asexual and sexual reproduction can lead to tandem repeat elongation in the target gene of the azoles: the cyp51A gene. In this review, we will explain how the fungus can generate genetic variation that can lead to adaptation. We will discuss recent advances that have been made in the understanding of the lifecycle of A. fumigatus to explain the differences observed in speed and type of mutations that are generated under different environments and how this can facilitate adaptation, such as azole-resistance selection.
Highlights
Aspergillus fumigatus is a filamentous fungus that can cause human diseases ranging from allergic bronchopulmonary aspergillosis to chronic pulmonary aspergillosis or even life-threatening acute invasive aspergillosis (IA)
We review what is currently known of the lifecycle of A. fumigatus in relation to various environments
We focus on the various aspects of the lifecycle and their relevance for contributing to adaptive genetic variation by mutation and recombination under the different environmental conditions
Summary
Aspergillus fumigatus is a filamentous fungus that can cause human diseases ranging from allergic bronchopulmonary aspergillosis to chronic pulmonary aspergillosis or even life-threatening acute invasive aspergillosis (IA). In immune-competent individuals, airway epithelial cells and resident alveolar macrophages remove inhaled conidia; in individuals who are unable to clear these conidia, germination could occur, subsequently leading to Aspergillus disease [2]. Among the infections caused by Aspergillus species, A. fumigatus is the leading etiological agent in most geographic regions. In order to successfully infect or colonize human hosts, A. fumigatus may initially establish lung colonization due to its physiological versatility and can subsequently adapt, through genetic changes, to the human lung environment and stressors, such as antifungal agents. The particular genetic changes themselves leading to adaptation, such as antifungal resistance in the host [10,11]. We discuss the implications of genetic variation for azole resistance, a selection factor found both in human medicine and the environment
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