The complete genome sequence of Yersinia pseudotuberculosis IP31758, the causative agent of Far East scarlet-like fever.
The complete genome sequence of Yersinia pseudotuberculosis IP31758, the causative agent of Far East scarlet-like fever.
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Yersinia pseudotuberculosis IP31758的完整基因组序列，远东猩红热发烧的病因。
DOI：
10.1371/journal.pgen.0030142
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发表时间：
2007-08
期刊：
影响因子：
4.5
通讯作者：
Ravel, Jacques
中科院分区：
文献类型：
--
作者：
Eppinger, Mark;Rosovitz, M. J.;Fricke, Wolfgang Florian;Rasko, David A.;Kokorina, Galina;Fayolle, Corinne;Lindler, Luther E.;Carniel, Elisabeth;Ravel, Jacques
第一次报告的远东猩红热（FESLF）流行病于20世纪50年代末席卷了俄罗斯的太平洋沿岸地区。严重感染的症状包括皮疹和脱屑、脱屑、舌充血和中毒性休克综合征。术语FESLF是为感染而创造的，因为它与A组链球菌引起的猩红热具有相同的临床表现。致病因子后来被确定为假结核耶尔森氏菌，尽管发病率的范围与经典的假结核症状有很大不同。为了了解FESLF独特临床特征的起源和出现，我们对FESLF致病菌株Y的基因组进行了测序。pseudotuberculosis IP 31758与另一株Y.假结核菌株，IP 32953，其引起典型的胃肠道症状。假结核Y菌IP 31758的独特基因库包含260多个菌株特异性基因，并引入了个体生理能力和毒力决定因子，其中很大一部分可能来自肠杆菌科和其他在同一生态位中持续存在的土壤细菌。该移动的基因组库包括两种与目前报道的所有耶尔森氏菌质粒在遗传学上无关的新质粒。icm/dot型IVB分泌系统，仅与军团菌目的细胞内持续病原体共享，在较大质粒上发现，由于引入免疫调节和免疫抑制能力，可能导致患者出现猩红热症状。我们确定了耶尔森氏菌属内基因组进化和物种形成所导致的共同和独特性状，并绘制了耶尔森氏菌属与耶尔森氏菌属之间更准确的物种边界。pseudotuberculosis和Y.鼠疫与进化中年轻的下行Y.鼠疫菌的群体遗传学研究;假结核病的异质性更强。两个Y.假结核菌株IP 31758和先前测序的Y.假结核菌株IP 32953已经通过获得特异性质粒以及通过水平获得不同的遗传信息并将其并入染色体中而进化，这两者一起或独立地似乎潜在地影响这两种菌株的表型适应。我们分析了一个Y染色体的基因组序列。引起远东猩红热（FESLF）的假结核分离株。FESLF导致严重的临床表现，包括猩红样皮疹，这种疾病由此得名，最重要的是，在常见的假结核感染中未见中毒性休克综合征。这项研究的目的是对基因组目录进行编目，并深入了解这种疾病的起源和出现。耶尔森氏菌属包括另外两种引起人类和动物感染的病原体：小肠结肠炎，如Y.假结核病会导致胃肠道疾病，而鼠疫耶尔森氏菌是鼠疫（也称为“黑死病”）的病原体。通过比较这三种耶尔森菌的基因组，我们可以确定几个独特的毒力决定因素，其中许多是已知的触发和调节宿主免疫系统的反应，并可能与严重的和非典型的FESLF临床表现密切相关。我们已经证明了Y.鼠疫从肠道致病菌Y.假结核病并不像最初认为的那样广泛。另一方面，我们的分析表明，基因获得是影响Y。假结核基因组进化
The first reported Far East scarlet-like fever (FESLF) epidemic swept the Pacific coastal region of Russia in the late 1950s. Symptoms of the severe infection included erythematous skin rash and desquamation, exanthema, hyperhemic tongue, and a toxic shock syndrome. The term FESLF was coined for the infection because it shares clinical presentations with scarlet fever caused by group A streptococci. The causative agent was later identified as Yersinia pseudotuberculosis, although the range of morbidities was vastly different from classical pseudotuberculosis symptoms. To understand the origin and emergence of the peculiar clinical features of FESLF, we have sequenced the genome of the FESLF-causing strain Y. pseudotuberculosis IP31758 and compared it with that of another Y. pseudotuberculosis strain, IP32953, which causes classical gastrointestinal symptoms. The unique gene pool of Y pseudotuberculosis IP31758 accounts for more than 260 strain-specific genes and introduces individual physiological capabilities and virulence determinants, with a significant proportion horizontally acquired that likely originated from Enterobacteriaceae and other soil-dwelling bacteria that persist in the same ecological niche. The mobile genome pool includes two novel plasmids phylogenetically unrelated to all currently reported Yersinia plasmids. An icm/dot type IVB secretion system, shared only with the intracellular persisting pathogens of the order Legionellales, was found on the larger plasmid and could contribute to scarlatinoid fever symptoms in patients due to the introduction of immunomodulatory and immunosuppressive capabilities. We determined the common and unique traits resulting from genome evolution and speciation within the genus Yersinia and drew a more accurate species border between Y. pseudotuberculosis and Y. pestis. In contrast to the lack of genetic diversity observed in the evolutionary young descending Y. pestis lineage, the population genetics of Y. pseudotuberculosis is more heterogenous. Both Y. pseudotuberculosis strains IP31758 and the previously sequenced Y. pseudotuberculosis strain IP32953 have evolved by the acquisition of specific plasmids and by the horizontal acquisition and incorporation of different genetic information into the chromosome, which all together or independently seems to potentially impact the phenotypic adaptation of these two strains. We have analyzed the genome sequence of a Y. pseudotuberculosis isolate responsible for Far East scarlet-like fever (FESLF). FESLF leads to severe clinical manifestations, including scarlet-like skin rash, from which this illness gets its name, and, most importantly, a toxic shock syndrome not seen in common pseudotuberculosis infections. The aim of this study was to catalogue the genomic inventory and get insights in the origin and emergence of this disease. The genus Yersinia comprises two other pathogens that cause worldwide infections in humans and animals: Y. enterocolitica, like Y. pseudotuberculosis, causes gastrointestinal disorders, while Yersinia pestis is the causative agent of plague, also known as the “Black Death.” By comparing the genome of these three Yersinia species, we could identify several unique virulence determinants, many of which are known to trigger and modulate the host immune system response and may be intimately associated with the severe and atypical FESLF clinical presentations. We have shown that the reductive gene loss process that Y. pestis has undergone since emerging from the enteric pathogen Y. pseudotuberculosis is not as extensive as originally thought. On the other hand, our analysis indicates that gene acquisition is a major factor that influenced Y. pseudotuberculosis genome evolution.
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影响因子：
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