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Zoonotic Microsporidia: Host Regulation and Pathogenesis

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Zoonotic Microsporidia: Host Regulation and Pathogenesis

Author Information
1
The State Key Laboratory of Resource Insects, Southwest University, Chongqing 400715, China
2
Chongqing Key Laboratory of Microsporidia Infection and Control, Southwest University, Chongqing 400715, China
*
Authors to whom correspondence should be addressed.

Received: 24 April 2026 Revised: 18 May 2026 Accepted: 04 June 2026 Published: 08 June 2026

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© 2026 The authors. This is an open access article under the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).

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Fungal Res. 2026, 1(1), 10003; DOI: 10.70322/fungalres.2026.10003
ABSTRACT: Microsporidia are a group of obligate intracellular fungal pathogens with extremely wide host ranges. Among these, zoonotic microsporidia such as Encephalitozoon hellem, Encephalitozoon cuniculi, and Enterocytozoon bieneusi can infect humans as well as other animals, causing recurrent diarrhea, hepatitis, and even death in immune-compromised individuals. The abilities of zoonotic microsporidia to regulate their hosts are essential to their survival and thriving within hosts. The manipulations of zoonotic microsporidia on hosts are employed in multiple ways, including metabolic modulation, immune suppression, signaling pathway regulations, and epigenetic modification. This review focuses on pathogen-host interactions between zoonotic microsporidia and their hosts, and compares their regulatory characteristics with those of typical fungal pathogens such as Candida albicans. In summary, unraveling the regulatory strategies of zoonotic microsporidia not only deepens our understanding of microsporidia pathogenesis but also provides potential targets for therapeutic intervention against these emerging pathogens. Comparative studies with typical fungal pathogens further highlight the unique and sophisticated host-manipulating mechanisms evolved by microsporidia from the fungal kingdom.
Keywords: Zoonotic microsporidia; Metabolism; Signaling pathways; Immunity; Epigenetics
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