白色念珠菌的學名Candida albicans為一同義反覆,其中屬名Candida來自拉丁文的candidus,意指白色,種小名albicans來自拉丁文的albicō,意思亦為白色[22]。早在西元前400年,希波克拉底在其著作《論流行病》(Of the Epidemics)中即提到了鵝口瘡,可能是白色念珠菌感染的最早記載[2][23]。
單倍體的白色念珠菌的基因組的大小約為15Mb(雙倍體約為29Mb)[29],由8條染色體對組成,二倍體中其中一組染色體分別稱為chr1A、chr2A、chr3A、chr4A、chr5A、chr6A、chr7A和chrRA,另一組染色體具有相似的名稱,但最後一個字為B,如chr1B、chr2B、...和chrRB。整個基因組包含6198個開放閱讀框(ORF),截至2019年2月,這些ORF中仍有70%尚未被鑑定[30]。有研究使用四環素轉錄調控系統控制白色念珠菌各個基因的表現,建構了一個GRACE(基因置換和條件表達)資料庫,研究白色念珠菌基因組中各基因對其生長的必要性,結果顯示其中有567個基因是其生長所必須的[31][32]。研究白色念珠菌最常用的菌株是WO-1和SC5314菌株,WO-1菌株可高頻率地在白色型(white)與混濁型(opaque)之間互相轉換,而SC5314菌株是用作基因組參考序列的菌株[33]。白色念珠菌兩種常用菌株的基因組已經完成全基因組定序[8],其中SC5314菌株完成於2004年[34],是較早完成測序的真菌(英語:List of sequenced fungi genomes)之一。
酵母菌型-菌絲型轉換對白色念珠菌的致病能力相當重要。吞噬細胞是宿主抗真菌免疫反應中的重要環節,白色念珠菌被巨噬細胞內吞後,並由酵母菌型轉換為菌絲型,最終穿透巨噬細胞而重新回到組織中。在巨噬細胞內部,白色念珠菌會啟動許多基因的表現,改變其代謝與促進型態轉換,其中許多基因為念珠菌所特有,釀酒酵母中不存在同源基因者,很可能與白色念珠菌的致病能力有關[85]。另外菌絲型的白色念珠菌菌絲表面有Hwp1(英語:Hwp1)(Hyphal wall protein 1)蛋白,該蛋白可與宿主上皮細胞表面的轉麩醯胺酶(英語:Transglutaminase)結合,有助白色念珠菌黏附於宿主細胞,進而造成感染[86]。
McClary, Dan Otho. Factors Affecting the Morphology of Candida Albicans. Annals of the Missouri Botanical Garden. May 1952, 39 (2): 137–164. JSTOR 2394509. doi:10.2307/2394509.
Geraldine Butler, Matthew D. Rasmussen, Christina A. Cuomo. Evolution of pathogenicity and sexual reproduction in eight Candida genomes. Nature. 2009, 459 (7247): 657-662. doi:10.1038/nature08064.
M. A. Pfaller, D. J. Diekema. Epidemiology of Invasive Candidiasis: a Persistent Public Health Problem. Clinical Microbiology Reviews. 2007, 20 (1): 133-163. doi:10.1128/CMR.00029-06.
Frans M. Klis, Chris G. de Koster, Stanley Brul. Cell Wall-Related Bionumbers and Bioestimates of Saccharomyces cerevisiae and Candida albicans. Eukaryot Cell. 2014, 13 (1): 2–9. doi:10.1128/EC.00250-13.
Christina M. Hull, Ryan M. Raisner, Alexander D. Johnson. Evidence for Mating of the "Asexual" Yeast Candida albicans in a Mammalian Host. Science. 2000, 289 (5477): 307-310. doi:10.1126/science.289.5477.307.
Stefanie Mühlhausen, Martin Kollmar. Molecular Phylogeny of Sequenced Saccharomycetes Reveals Polyphyly of the Alternative Yeast Codon Usage. Genome Biol Evol. 2014, 6 (12): 3222–3237. doi:10.1093/gbe/evu152.
Ted Jones, Nancy A. Federspiel, Hiroji Chibana, Jan Dungan, Sue Kalman, B. B. Magee, George Newport,Yvonne R. Thorstenson, Nina Agabian, P. T. Magee, Ronald W. Davis, Stewart Scherer. The diploid genome sequence of Candida albicans. PNAS. 2004, 101 (19): 7329–7334. doi:10.1073/pnas.0401648101.
Andrzej (Anjay) Elzanowski and Jim Ostell. The Alternative Yeast Nuclear Code. The Genetic Codes. Bethesda, Maryland, U.S.A.: National Center for Biotechnology Information (NCBI). 2010-07-07 [2011-10-30]. (原始內容存檔於2011-05-13).
Santos, MA; Cheesman, C; Costa, V; Moradas-Ferreira, P; Tuite, MF. Selective advantages created by codon ambiguity allowed for the evolution of an alternative genetic code in Candida spp.. Molecular Microbiology. February 1999, 31 (3): 937–947. PMID 10048036. doi:10.1046/j.1365-2958.1999.01233.x.
Maria C. Costanzo, Martha B. Arnaud, Marek S. Skrzypek, Gail Binkley, Christopher Lane, Stuart R. Miyasato, Gavin Sherlock. The Candida Genome Database: Facilitating research on Candida albicans molecular biology. FEMS Yeast Research. 2006, 6 (5): 671-684. doi:10.1111/j.1567-1364.2006.00074.x.
Swoboda RK, Broadbent ID, Bertram G, Budge S, Gooday GW, Gow NA, Brown AJ. Structure and regulation of a Candida albicans RP10 gene which encodes an immunogenic protein homologous to Saccharomyces cerevisiae ribosomal protein 10. J Bacteriol. 1995, 177 (5): 1239-1246. doi:10.1128/jb.177.5.1239-1246.1995.
Abdul Munir Abdul Murad, Philip R. Lee, Ian D. Broadbent, Caroline J. Barelle, Alistair J. P. Brown. CIp10, an efficient and convenient integrating vector for Candida albicans. Yeast. 2000, 14 (4): 325-327. doi:10.1002/1097-0061(20000315)16:4<325::AID-YEA538>3.0.CO;2-%23.
Suzanne M Noble, Sarah French, Lisa A Kohn, Victoria Chen, Alexander D Johnson. Systematic screens of a Candida albicanshomozygous deletion library decouple morphogenetic switching and pathogenicity. Nature Genetics. 2010, 42 (7): 590–598. doi:10.1038/ng.605.
Peter Staib, Joachim Morschhäuser. Chlamydospore formation in Candida albicans and Candida dubliniensis– an enigmatic developmental programme. Mycoses. 2006, 50 (1): 1-12. doi:10.1111/j.1439-0507.2006.01308.x.
José Pérez‐Martín, José Antonio Uría, Alexander D. Johnson. Phenotypic switching in Candida albicans is controlled by a SIR2 gene. The EMBO Journal. 1999, 18 (9): 2580-2592. doi:10.1093/emboj/18.9.2580.
Guanghua Huang, Song Yi, Nidhi Sahni, Karla J. Daniels, Thyagarajan Srikantha, David R. Soll. N-Acetylglucosamine Induces White to Opaque Switching, a Mating Prerequisite in Candida albicans. PLoS Pathogens. 2010, 6 (3): e1000806. doi:10.1371/journal.ppat.1000806.
Li Tao, Han Du, Guobo Guan, Yu Dai, Clarissa J. Nobile, Weihong Liang, Chengjun Cao, Qiuyu Zhang, Jin Zhong, Guanghua Huang. Discovery of a “White-Gray-Opaque” Tristable Phenotypic Switching System in Candida albicans: Roles of Non-genetic Diversity in Host Adaptation. PLoS Biology. 2014, 12 (4): e1001830. doi:10.1371/journal.pbio.1001830.
Kevin Alby, Richard J. Bennett. Sexual reproduction in the Candida clade: cryptic cycles, diverse mechanisms, and alternative functions. Cell Mol Life Sci.. 2010, 67 (19): 3275–3285. doi:10.1007/s00018-010-0421-8.
Yang-Nim Park, Karla J. Daniels, Claude Pujol, Thyagarajan Srikantha, David R. Soll. Candida albicans Forms a Specialized “Sexual” as Well as “Pathogenic” Biofilm. Eukaryotic Cell. 2013, 12 (8): 1120-1131. doi:10.1128/EC.00112-13.
Anja Forche, Kevin Alby, Dana Schaefer, Alexander D Johnson, Judith Berman, Richard J Bennett. The Parasexual Cycle in Candida albicans Provides an Alternative Pathway to Meiosis for the Formation of Recombinant Strains. PLoS Biology. 2008, 6 (5): e110. doi:10.1371/journal.pbio.0060110.
Richard J. Bennett, Alexander D. Johnson. Completion of a parasexual cycle in Candida albicans by induced chromosome loss in tetraploid strains. The EMBO Journal: 2505-2515. doi:10.1093/emboj/cdg235.
Meleah A. Hickman, Guisheng Zeng, Anja Forche, Matthew P. Hirakawa, Darren Abbey, Benjamin D. Harrison, Yan-Ming Wang, Ching-hua Su, Richard J. Bennett, Yue Wang, Judith Berman. The ‘obligate diploid’ Candida albicansforms mating-competent haploids. Nature. 2013, 494 (7435): 55-59. doi:10.1038/nature11865.
Monika S, Małgorzata B, Zbigniew O. Contribution of Aspartic Proteases in Candida Virulence. Protease Inhibitors against Candida Infections. Curr Protein Pept Sci.. 2017, 18 (10): 1050-1062. doi:10.2174/1389203717666160809155749.
Clarissa J. Nobile, Emily P.Fox, Jeniel E.Nett, Trevor R. Sorrells, Quinn M. Mitrovich, Aaron D. Hernday, Brian B. Tuch, David R.Andes, Alexander D. Johnson. A Recently Evolved Transcriptional Network Controls Biofilm Development in Candida albicans. Cell. 2012, 148 (1-2): 126-138. doi:10.1016/j.cell.2011.10.048.
Clarissa J. Nobile and Alexander D. Johnson. Candida albicans Biofilms and Human Disease. Annu Rev Microbiol.. 2015, 69: 71-92. doi:10.1146/annurev-micro-091014-104330.
Emily R. M. Sydnor, Trish M. Perl. Hospital Epidemiology and Infection Control in Acute-Care Settings. Clinical Microbioly Review. 2011, 24 (1): 141–173. doi:10.1128/CMR.00027-10.
Ilkit, M; Guzel, AB. The epidemiology, pathogenesis, and diagnosis of vulvovaginal candidosis: a mycological perspective. Critical Reviews in Microbiology. August 2011, 37 (3): 250–61. PMID 21599498. doi:10.3109/1040841X.2011.576332.
Weinberger, M. Characteristics of candidaemia with Candida-albicans compared with non-albicans Candida species and predictors of mortality. J Hosp Infect. 2016-04-16, 61 (2): 146–54. PMID 16009456. doi:10.1016/j.jhin.2005.02.009.