近日中國科學(xué)院病原微生物與免疫學(xué)重點實驗室朱寶利課題組、高福課題組與南京軍區(qū)疾病預(yù)防控制中心微生物流行病學(xué)研究所唐佳琪課題組展開合作,，深入研究了并揭示了豬鏈球菌的致病機理及其進化機制,。該研究成果對促進豬鏈球菌病的預(yù)防、監(jiān)測和控制具有重要指導(dǎo)意義。相關(guān)研究論文發(fā)表在《BMC Genomics》雜志上。
豬鏈球菌是一類重要的人畜共患病病原菌，可誘發(fā)豬的關(guān)節(jié)炎,、腦膜炎、肺炎,；還可引起人,、牛、馬,、羊,、禽等多種動物感染，可能造成病人腦膜炎,、聽力喪失,、敗血癥甚至死亡。1998至1999年江蘇省部分地區(qū)暴發(fā)該病,，造成25人感染發(fā)病,，其中14人死亡；2005年6月四川大規(guī)模暴發(fā)該病,，報告病例215例,，死亡38人。兩次暴發(fā)不僅造成養(yǎng)豬業(yè)的重大損失,，而且給人類健康構(gòu)成巨大威脅,。研究表明，中毒性休克綜合癥是這兩次豬鏈球菌暴發(fā)引起人群高死亡率（22.1%）的原因,。然而,，引起豬鏈球菌新臨床癥狀——中毒性休克綜合癥的原因尚不清楚。
在這篇文章中,，研究團隊利用比較基因組學(xué)技術(shù),，對引起中毒休克綜合癥的高毒豬鏈球菌進行了比較基因組學(xué)方法的研究。通過比較不同毒力,、不同來源的豬鏈球菌菌株基因組,，研究人員發(fā)現(xiàn)豬鏈球菌的基因組高度可變，而且引起兩次暴發(fā)的菌株均獲得了大量外源基因,。在其基因組上獲得的一段長約89kb的序列具有毒力島（Pathogenicity island）的顯著特征,，毒力島內(nèi)的ABC型轉(zhuǎn)運系統(tǒng)和SalK/R雙信號轉(zhuǎn)導(dǎo)系統(tǒng)為引起中毒休克綜合癥菌株的特異基因,。前期研究表明，豬鏈球菌缺乏引起中毒性休克綜合癥的所需的超抗原和M蛋白的類似物,，據(jù)此推測,，由ABC型轉(zhuǎn)運系統(tǒng)排出的某類物質(zhì)可能正是引起中毒休克綜合癥的元兇。此外,，通過比較基因組分析,，研究人員發(fā)現(xiàn)基因獲得和基因重排是豬鏈球菌微進化的主要動因，研究團隊據(jù)此提出豬鏈球微進化模型,。同時，在該研究中還發(fā)現(xiàn)了多個豬鏈球菌致病的候選基因,，這些候選基因為尋找豬鏈球菌進化后的毒力基因簇提供了參考,。（生物谷Bioon.com）
生物谷推薦原文出處：
BMC Genomics DOI:10.1186/1471-2164-12-219
Probing genomic diversity and evolution of Streptococcus suis serotype 2 by NimbleGen tiling arrays
Zuowei Wu , Ming Li , Changjun Wang , Jing Li , Na Lu , Ruifen Zhang , Yongqiang Jiang , Ruifu Yang , Cuihua Liu , Hui Liao , George F Gao , Jiaqi Tang and Baoli Zhu
Background
Our previous studies revealed that a new disease form of streptococcal toxic shock syndrome (STSS) is associated with specific Streptococcus suis serotype 2 (SS2) strains. To achieve a better understanding of the pathogenicity and evolution of SS2 at the whole-genome level, comparative genomic analysis of 18 SS2 strains, selected on the basis of virulence and geographic origin, was performed using NimbleGen tiling arrays.
Results
Our results demonstrate that SS2 isolates have highly divergent genomes. The 89K pathogenicity island (PAI), which has been previously recognized as unique to the Chinese epidemic strains causing STSS, was partially included in some other virulent and avirulent strains. The ABC-type transport systems, encoded by 89K, were hypothesized to greatly contribute to the catastrophic features of STSS. Moreover, we identified many polymorphisms in genes encoding candidate or known virulence factors, such as PlcR, lipase, sortases, the pilus-associated proteins, and the response regulator RevS and CtsR. On the basis of analysis of regions of differences (RDs) across the entire genome for the 18 selected SS2 strains, a model of microevolution for these strains is proposed, which provides clues into Streptococcus pathogenicity and evolution.
Conclusions
Our deep comparative genomic analysis of the 89K PAI present in the genome of SS2 strains revealed details into how some virulent strains acquired genes that may contribute to STSS, which may lead to better environmental monitoring of epidemic SS2 strains.
