近日中国科学院病原微生物与免疫学重点实验室朱宝利课题组、高福课题组与南京军区疾病预防控制中心微生物流行病学研究所唐佳琪课题组展开合作，深入研究了并揭示了猪链球菌的致病机理及其进化机制。该研究成果对促进猪链球菌病的预防、监测和控制具有重要指导意义。相关研究论文发表在《BMC Genomics》杂志上。
猪链球菌是一类重要的人畜共患病病原菌，可诱发猪的关节炎、脑膜炎、肺炎；还可引起人、牛、马、羊、禽等多种动物感染，可能造成病人脑膜炎、听力丧失、败血症甚至死亡。1998至1999年江苏省部分地区暴发该病，造成25人感染发病，其中14人死亡；2005年6月四川大规模暴发该病，报告病例215例，死亡38人。两次暴发不仅造成养猪业的重大损失，而且给人类健康构成巨大威胁。研究表明，中毒性休克综合症是这两次猪链球菌暴发引起人群高死亡率（22.1%）的原因。然而，引起猪链球菌新临床症状——中毒性休克综合症的原因尚不清楚。
在这篇文章中，研究团队利用比较基因组学技术，对引起中毒休克综合症的高毒猪链球菌进行了比较基因组学方法的研究。通过比较不同毒力、不同来源的猪链球菌菌株基因组，研究人员发现猪链球菌的基因组高度可变，而且引起两次暴发的菌株均获得了大量外源基因。在其基因组上获得的一段长约89kb的序列具有毒力岛（Pathogenicity island）的显著特征，毒力岛内的ABC型转运系统和SalK/R双信号转导系统为引起中毒休克综合症菌株的特异基因。前期研究表明，猪链球菌缺乏引起中毒性休克综合症的所需的超抗原和M蛋白的类似物，据此推测，由ABC型转运系统排出的某类物质可能正是引起中毒休克综合症的元凶。此外，通过比较基因组分析，研究人员发现基因获得和基因重排是猪链球菌微进化的主要动因，研究团队据此提出猪链球微进化模型。同时，在该研究中还发现了多个猪链球菌致病的候选基因，这些候选基因为寻找猪链球菌进化后的毒力基因簇提供了参考。（生物谷Bioon.com）
生物谷推荐原文出处：
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.
