Cited by 1,848Antifungal resistance and susceptibilityFungal and yeast genetics researchFungal Infections and Studies

The DOI matches its Crossref record; 136 of the 136 references it cites were found in a registry or an index.

Candida albicans pathogenicity mechanisms

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Abstract

The polymorphic fungus Candida albicans is a member of the normal human microbiome. In most individuals, C. albicans resides as a lifelong, harmless commensal. Under certain circumstances, however, C. albicans can cause infections that range from superficial infections of the skin to life-threatening systemic infections. Several factors and activities have been identified which contribute to the pathogenic potential of this fungus. Among them are molecules which mediate adhesion to and invasion into host cells, the secretion of hydrolases, the yeast-to-hypha transition, contact sensing and thigmotropism, biofilm formation, phenotypic switching and a range of fitness attributes. Our understanding of when and how these mechanisms and factors contribute to infection has significantly increased during the last years. In addition, novel virulence mechanisms have recently been discovered. In this review we present an update on our current understanding of the pathogenicity mechanisms of this important human pathogen.

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Crossref · 10.4161/viru.22913

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Figures

Figure 1. An overview of selected C. albicans pathogenicity mechanisms. Yeast cells adhere to host cell surfaces by the expression of adhesins. Contact to host cells triggers the yeast-to-hypha transition and directed growth via thigmotropism. The expression of invasins mediates uptake of the fungus by the host cell through induced endocytosis. Adhesion, physical forces and secretion of fungal hydrolases has been proposed to facilitate the second mechanism of invasion, i.e., fungal-driven active penetration into host cells by breaking down barriers. The attachment of yeast cells to abiotic (e.g., catheters) or biotic (host cells) surfaces can give rise to the formation of biofilms with yeast cells in the lower part and hyphal cells in the upper part of the biofilm. Phenotypic plasticity (switching) has been proposed to influence antigenicity and biofilm formation of C. albicans. In addition to these virulence factors, several fitness traits influence fungal pathogenicity. They include a robust stress response mediated by heat shock proteins (Hsps); auto-induction of hyphal formation through uptake of amino acids, excretion of ammonia (NH3) and concomitant extracellular alkalinization; metabolic flexibility and uptake of different compounds as carbon (C) and nitrogen (N) sources; and uptake of essential trace metals, e.g., iron (Fe), zinc (Zn), copper (Cu) and manganese (Mn).
Figure 1. An overview of selected C. albicans pathogenicity mechanisms. Yeast cells adhere to host cell surfaces by the expression of adhesins. Contact to host cells triggers the yeast-to-hypha transition and directed growth via thigmotropism. The expression of invasins mediates uptake of the fungus by the host cell through induced endocytosis. Adhesion, physical forces and secretion of fungal hydrolases has been proposed to facilitate the second mechanism of invasion, i.e., fungal-driven active penetration into host cells by breaking down barriers. The attachment of yeast cells to abiotic (e.g., catheters) or biotic (host cells) surfaces can give rise to the formation of biofilms with yeast cells in the lower part and hyphal cells in the upper part of the biofilm. Phenotypic plasticity (switching) has been proposed to influence antigenicity and biofilm formation of C. albicans. In addition to these virulence factors, several fitness traits influence fungal pathogenicity. They include a robust stress response mediated by heat shock proteins (Hsps); auto-induction of hyphal formation through uptake of amino acids, excretion of ammonia (NH3) and concomitant extracellular alkalinization; metabolic flexibility and uptake of different compounds as carbon (C) and nitrogen (N) sources; and uptake of essential trace metals, e.g., iron (Fe), zinc (Zn), copper (Cu) and manganese (Mn).CC BY-NC · PubMed Central

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Research works printed but not linked: 3

  1. Ruhnke M. Skin and mucous membrane infections. In: Calderone RA, ed. Candida and Candidiasis: ASM Press, Washington, DC, pp. 307-325., 2002.
  2. Zordan R, Cormack B. Adhesins on Opportunistic Fungal Pathogens. In: Calderone RA, Clancy, C.J., ed. Candida and Candidiasis: ASM Press, Washington, DC, pp 243-259, 2012.
  3. Brown AJP, Haynes K, Gow NAR, Quinn J. Stress Responses in Candida . In: Calderone RA, Clancy, C.J., ed. Candida and Candidiasis: ASM Press, Washington, DC, pp. 225-242., 2012.

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Metadata

Authors
Mayer, F. L., Wilson, D., & Hube, B.
Affiliations
  • Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) (DE)
  • Jena University Hospital (DE)
Corresponding author
Hube, Bernhard
Venue
Virulence
Published
2013-02-15
Volume
4
Issue
2
Pages
119-128
ISSN
  • 2150-5594 (ISSN-L)
  • 2150-5608
OpenAlex
W2144035662
Cited by
1,848
References
136
Citations by year
2026: 99 · 2025: 162 · 2024: 163 · 2023: 180 · 2022: 195 · 2021: 189 · 2020: 164 · 2019: 156 · 2018: 150 · 2017: 119 · 2016: 97 · 2015: 84 · 2014: 57 · 2013: 30
FWCI
11.35
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Virulence (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Aberdeen University Research Archive (Aberdeen University) (submittedVersion)
Funders
  • Deutsche Forschungsgemeinschaft (01EO1002)
  • Bundesministerium für Bildung und Forschung (01EO1002)
  • International Leibniz Research School for Microbial and Biomolecular Interactions
  • Leibniz-Gemeinschaft
  • Center for Sepsis Control and Care (BMBF 01EO1002, 01EO1002)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Health Sciences › Medicine › Infectious Diseases › Fungal Infections and Studies
Keywords
Candida albicans, fungal pathogenicity, virulence factors, host cell invasion, yeast-to-hypha transition, tactile sensing, thigmotropism, biofilm formation, phenotypic switching, commensal to pathogen transition, systemic candidiasis, superficial fungal infections
MeSH terms
Candida albicans, Candidiasis, Humans, Virulence Factors

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