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. 2023 Mar 17;12:20. doi: 10.1186/s40249-023-01073-4

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Antifungals, targets, and antifungal resistance mechanism. Three main classes of drugs are used in the treatment of cryptococcal infections: polyenes (AmB), azoles (fluconazole), flucytosine. C. neoformans is intrinsic resistant to echinocandins (shown in dotted lines). AmB binds to ergosterol in the cell membrane, which forming pores and exerting fungicidal activity. Fluconazole targets the ergosterol biosynthetic enzyme Erg11. Flucytosine blocks DNA synthesis. C. neoformans cells develop resistance to different drugs through different mechanisms. The exact mechanism leading to AmB resistance is not yet clear. Fluconazole resistance has been reported to be associated with aneuploidy, heteroresistance and mutations in the ERG11 gene. Flucytosine resistance may be associated with mutations in genes related to flucytosine conversion, hypermutation, and transposon mutagenesis. The echinocandins resistance is attributed to the interaction of Cdc50 and Crm1, and preventing drug uptake could also arise echinocandins resistance