Wickes B L, Petter R
Department of Laboratory Medicine, University of California, San Francisco 94143-0626, USA.
Curr Top Med Mycol. 1996 Dec;7(1):71-86.
Candida albicans displays many types of variation which affect a broad spectrum of phenotypes. Among them are antigenic, chromosomal, morphologic, and biochemical variation. The ability to modulate many phenotypes is clearly an important factor in the success of this fungus as a pathogen and variation at the genomic level may be the common denominator among the different systems. Genomic variation in C. albicans has been studied by many researchers and a number of different mechanisms have been identified. Among them are ploidy fluctuations, which allow the organism to cycle from 2n chromosome number to 4n or higher; translocation, which has been demonstrated to involve many different chromosomes and affects many phenotypes including virulence; mitotic recombination, which has been demonstrated to increase resistance to certain drugs; and nondisjunction, which has been shown to have morphological consequences. The number and diversity of these mechanisms combine to make C. albicans a highly successful organism. Although normally a commensal of humans, when invasive, C. albicans can inhabit almost any site in the body. It is not known what governs the transition of C. albicans from a commensal to pathogenic invader, however, variation at the genomic level likely plays a role. One possible consequence of variation is the generation of atypical strains, further expanding the documented phenotypic plasticity of this organism. The exposure of patients to cytotoxic drugs during treatment of such diseases as AIDS or cancer increases the selective pressure and has exacerbated both the frequency and degree of variability observed in C. albicans. The molecular analysis of genomic variation in C. albicans is proving to be a fertile area of research and future investigations can only be expected to add to the mechanisms documented in this review.
白色念珠菌表现出多种类型的变异，这些变异影响广泛的表型。其中包括抗原性、染色体、形态学和生化变异。调节多种表型的能力显然是这种真菌作为病原体成功的一个重要因素，而基因组水平的变异可能是不同系统中的共同因素。许多研究人员对白色念珠菌的基因组变异进行了研究，并确定了一些不同的机制。其中包括倍性波动，它使生物体能够从2n染色体数循环到4n或更高；易位，已证明其涉及许多不同的染色体，并影响包括毒力在内的许多表型；有丝分裂重组，已证明其可增加对某些药物的抗性；以及不分离，已证明其具有形态学后果。这些机制的数量和多样性共同使白色念珠菌成为一种非常成功的生物体。虽然白色念珠菌通常是人类的共生菌，但在侵入性感染时，它可以栖息在身体的几乎任何部位。然而，尚不清楚是什么控制着白色念珠菌从共生菌向致病性入侵者的转变，不过基因组水平的变异可能起到了一定作用。变异的一个可能后果是产生非典型菌株，这进一步扩大了该生物体已记录的表型可塑性。在治疗艾滋病或癌症等疾病期间，患者接触细胞毒性药物增加了选择压力，并加剧了白色念珠菌中观察到的变异频率和程度。对白色念珠菌基因组变异的分子分析已被证明是一个富有成果的研究领域，预计未来的研究只会增加本综述中记录的机制。
