Aspergillus fumigatus escape mechanisms from its harsh survival environments

Abstract

Aspergillus fumigatus is the main pathogenic fungus underlying aspergillosis and globally causes more than 300,000 life-threatening infections every year (Earl Kang and Celia 2021 ). Moreover, in recent years, during the Coronavirus 2019 (COVID-19) pandemic, pulmonary aspergillosis led to Aspergillus co-infections with COVID-19 developed into a clinical, major life-threatening fungal disease (Giacobbe et al. 2022 ; Hoenigl 2021 ). As a saprophytic fungal pathogen, A. fumigatus proliferates via abundant, small diameter (2–3 μm), air-borne asexual conidia. Although the fungus may encounter harsh natural conditions, such as high temperatures, poor carbon or nitrogen sources, ultraviolet light, and reduced metal ion levels, it has evolved adaptive survival systems. Generally, conidiophores generate thousands of conidia; indoor and outdoor airborne conidia concentrations can range from 1 to 100 conidia/m 3 and even reach up to 10 8 conidia/m 3 in certain environments (Latgé and Chamilos 2019 ). Moreover, abundant conidia are inhaled daily into human lungs (Furlong-Silva and Cook 2022 ). In immunocompetent hosts, approximately 90% of inhaled conidia are swiftly cleared at mucosal surfaces and ciliated cells in the respiratory tract. Residually activated and swollen conidia face hostile environments, including low carbon sources, low oxygen concentrations, and host immune responses (Margalit and Kavanagh 2015 ); therefore, A. fumigatus survival in healthy individuals poses challenges to the fungus. However, A. fumigatus can evade host defenses for the spores to germinate or proliferate and causes aspergillosis in immunocompromised and immunodeficient individuals (Verburg et al. 2022 ).

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