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<p>The alarming rise in fungal infections poses a serious health concern worldwide. <i>Candida albicans</i> is a highly virulent, ubiquitous opportunistic fungal pathogen associated with high mortality, particularly in immunocompromised individuals. Its infections range from superficial mucosal to invasive candidiasis. The pathogenicity of <i>C. albicans</i> is largely attributed to its ability to undergo phenotypic switching between different morphological forms ranging from unicellular to hyphae. A key factor in its pathogenesis is candidalysin, a fungal cytolytic peptide toxin. Candidalysin is generated through the expression of the <i>ECE1</i> polyprotein, which, upon cleavage by the protease Kex2, yields both candidalysin and non-candidalysin ECE1-derived peptides. Notably, despite its critical role in virulence, the <i>ECE1</i> gene is not widely conserved among fungal pathogens and is predominantly restricted to a few <i>Candida</i> species. This review highlights recent advances in understanding candidalysin-mediated cell damage and immune activation pathways, and also provides insights into the evolution of the <i>ECE1</i> gene and its potential role in the coevolution of <i>C. albicans</i> with its human host.</p>

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Insights into the evolution of Candidalysin and recent developments

  • 期刊论文

  • 发表日期：

    2025年7月31日

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  • Ananya Konwar,
  • Kartavya Mathur,
  • Shivam Pandey,
  • Kunjan Bhorali,
  • Anil Thakur,
  • Rekha Puria

摘要

The alarming rise in fungal infections poses a serious health concern worldwide. Candida albicans is a highly virulent, ubiquitous opportunistic fungal pathogen associated with high mortality, particularly in immunocompromised individuals. Its infections range from superficial mucosal to invasive candidiasis. The pathogenicity of C. albicans is largely attributed to its ability to undergo phenotypic switching between different morphological forms ranging from unicellular to hyphae. A key factor in its pathogenesis is candidalysin, a fungal cytolytic peptide toxin. Candidalysin is generated through the expression of the ECE1 polyprotein, which, upon cleavage by the protease Kex2, yields both candidalysin and non-candidalysin ECE1-derived peptides. Notably, despite its critical role in virulence, the ECE1 gene is not widely conserved among fungal pathogens and is predominantly restricted to a few Candida species. This review highlights recent advances in understanding candidalysin-mediated cell damage and immune activation pathways, and also provides insights into the evolution of the ECE1 gene and its potential role in the coevolution of C. albicans with its human host.