Tuchscherr Lorena, Löffler Bettina, Proctor Richard A
Institute of Medical Microbiology, Jena University Hospital, Jena, Germany.
Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany.
Front Microbiol. 2020 May 21;11:1028. doi: 10.3389/fmicb.2020.01028. eCollection 2020.
is able to survive within host cells by switching its phenotype to the small-colony variant (SCV) phenotype. The emergence of SCVs is associated with the development of persistent infections, which may be both chronic and recurrent. This slow-growing subpopulation of forms small colonies on solid-medium agar, is induced within host cells, presents a non-homogenous genetic background, has reduced expression of virulence factors and presents a variable phenotype (stable or unstable). While virtually all SCVs isolated from clinical specimens can revert to the parental state with rapid growth, the stable SCVs recovered in clinical specimens have been found to contain specific mutations in metabolic pathways. In contrast, other non-stable SCVs are originated from regulatory mechanisms involving global regulators (e.g., , , and ) or other non-defined mutations. One major characteristic of SCVs was the observation that SCVs were recovered from five patients with infections that could persist for decades. In these five cases, the SCVs had defects in electron transport. This linked persistent infections with SCVs. The term "persistent infection" is a clinical term wherein bacteria remain in the host for prolonged periods of time, sometimes with recurrent infection, despite apparently active antibiotics. These terms were described where bacteria remain viable in liquid culture medium in the presence of antibiotics. These bacteria are called "persisters". While SCVs can be persisters in liquid culture, not all persisters are SCVs. One mechanism associated with the metabolically variant SCVs is the reduced production of virulence factors. SCVs have consistently shown reduced levels of RNAIII, a product of the accessory gene regulatory () locus that controls a quorum-sensing system and regulates the expression of a large number of virulence genes. Reduced Agr acitivity is associated with enhanced survival of SCVs within host cells. In this review, we examine the impact of the SCVs with altered metabolic pathways on , and we draw distinctions with other types of SCVs that emerge within mammalian cells with prolonged infection.
通过将其表型转变为小菌落变体（SCV）表型，能够在宿主细胞内生存。SCV的出现与持续性感染的发展有关，持续性感染可能是慢性的且会复发。这种生长缓慢的亚群在固体培养基琼脂上形成小菌落，在宿主细胞内被诱导产生，具有非同质的遗传背景，毒力因子表达降低且呈现可变表型（稳定或不稳定）。虽然几乎所有从临床标本中分离出的SCV都能恢复到快速生长的亲代状态，但已发现临床标本中 recovered 的稳定SCV在代谢途径中含有特定突变。相比之下，其他非稳定SCV源自涉及全局调节因子（如 、 和 ）的调节机制或其他未明确的突变。SCV的一个主要特征是观察到从五名患有可能持续数十年感染的患者中分离出了SCV。在这五个病例中，SCV在电子传递方面存在缺陷。这将持续性感染与SCV联系起来。“持续性感染”是一个临床术语，指细菌在宿主中长时间存在，有时伴有反复感染，尽管使用了明显有效的抗生素。这些术语是在描述细菌在抗生素存在下在液体培养基中仍能存活的情况时提出的。这些细菌被称为“持续菌”。虽然SCV在液体培养中可以是持续菌，但并非所有持续菌都是SCV。与代谢变体SCV相关的一种机制是毒力因子产生减少。SCV一直显示RNAIII水平降低，RNAIII是辅助基因调节（）位点的产物，该位点控制群体感应系统并调节大量毒力基因的表达。Agr活性降低与SCV在宿主细胞内的存活率提高有关。在本综述中，我们研究了代谢途径改变的SCV对 的影响，并将其与在长时间感染的哺乳动物细胞中出现的其他类型SCV进行了区分。
原文中“recovered”处似乎有误，根据语境猜测可能是“isolated”之类的词，翻译时保留了原文错误。
