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孟加拉国达卡季节性霍乱暴发相关霍乱弧菌分离株的基因组动态。

Genome Dynamics of Vibrio cholerae Isolates Linked to Seasonal Outbreaks of Cholera in Dhaka, Bangladesh.

机构信息

International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b), Dhaka, Bangladesh.

International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b), Dhaka, Bangladesh

出版信息

mBio. 2020 Feb 11;11(1):e03339-19. doi: 10.1128/mBio.03339-19.

DOI:10.1128/mBio.03339-19
PMID:32047137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7018647/
Abstract

The temporal switching of serotypes from serotype Ogawa to Inaba and back to Ogawa was identified in O1, which was responsible for seasonal outbreaks of cholera in Dhaka during the period 2015 to 2018. In order to delineate the factors responsible for this serotype transition, we performed whole-genome sequencing (WGS) of O1 multidrug-resistant strains belonging to both the serotypes that were isolated during this interval where the emergence and subsequent reduction of the Inaba serotype occurred. The whole-genome-based phylogenetic analysis revealed clonal expansion of the Inaba isolates mainly responsible for the peaks of infection during 2016 to 2017 and that they might have evolved from the prevailing Ogawa strains in 2015 which coclustered with them. Furthermore, the gene in these Inaba serotype isolates was inactivated due to insertion of a transposable element at the same position signifying the clonal expansion. Also, isolates in the Inaba serotype dominant clade mainly contained classical allele and revealed differences in the genetic composition of eventh andemic sland II (VSP-II) and the SXT integrative and conjugative element (SXT-ICE) compared to those of Ogawa serotype strains which remerged in 2018. The variable presence of phage-inducible chromosomal island-like element 1 (PLE1) was also noted in the isolates of the Inaba serotype dominant clade. The detailed genomic characterization of the sequenced isolates has shed light on the forces which could be responsible for the periodic changes in serotypes of and has also highlighted the need to analyze the mobilome in greater detail to obtain insights into the mechanisms behind serotype switching. The switching of serotype from Ogawa to Inaba and back to Ogawa has been observed temporally in O1, which is responsible for endemic cholera in Bangladesh. The serospecificity is key for effective intervention and for preventing cholera, a deadly disease that continues to cause significant morbidity and mortality worldwide. In the present study, WGS of allowed us to better understand the factors associated with the serotype switching events observed during 2015 to 2018. Genomic data analysis of strains isolated during this interval highlighted variations in the genes , , and and also identified significant differences in the genetic content of the mobilome, which included key elements such as SXT ICE, VSP-II, and PLE. Our results indicate that selective forces such as antibiotic resistance and phage resistance might contribute to the clonal expansion and predominance of a particular serotype responsible for an outbreak.

摘要

血清型从 Ogawa 型到 Inaba 型再到 Ogawa 型的时间切换在 O1 中被发现,这是导致 2015 年至 2018 年期间达卡季节性霍乱爆发的原因。为了阐明导致这种血清型转变的因素,我们对属于这两种血清型的 O1 多药耐药菌株进行了全基因组测序 (WGS),这些菌株是在 Inaba 血清型出现和随后减少期间分离的。基于全基因组的系统发育分析显示,Inaba 分离株的克隆扩张主要负责 2016 年至 2017 年的感染高峰,它们可能是由 2015 年流行的 Ogawa 菌株进化而来的,这些菌株与它们聚集在一起。此外,这些 Inaba 血清型分离株中的 基因由于在相同位置插入转座元件而失活,表明了克隆扩张。此外,在 Inaba 血清型主导进化枝中的 分离株主要含有经典的 等位基因,并且与在 2018 年重新出现的 Ogawa 血清型菌株相比,在第二事件性流行岛 (VSP-II) 和 SXT 整合和共轭元件 (SXT-ICE) 的遗传组成上存在差异。在 Inaba 血清型主导进化枝中的分离株中还观察到噬菌体诱导的染色体岛样元件 1 (PLE1) 的可变存在。对测序分离株的详细基因组特征分析揭示了可能导致 周期性血清型变化的力量,并强调需要更详细地分析移动组以深入了解血清型转换背后的机制。血清型从 Ogawa 型到 Inaba 型再到 Ogawa 型的时间切换在 O1 中被观察到,这是孟加拉国地方性霍乱的原因。血清特异性是进行有效干预和预防霍乱的关键,霍乱是一种继续在全球造成重大发病率和死亡率的致命疾病。在本研究中,对 O1 的 WGS 使我们能够更好地理解与 2015 年至 2018 年期间观察到的血清型转换事件相关的因素。在这一期间分离的菌株的基因组数据分析突出了基因 、 、 和 的变化,并确定了移动组的遗传内容存在显著差异,其中包括 SXT ICE、VSP-II 和 PLE 等关键要素。我们的结果表明,抗生素耐药性和噬菌体耐药性等选择压力可能有助于导致爆发的特定 血清型的克隆扩张和优势。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/9e352e8c80c1/mBio.03339-19-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/cae7c679f246/mBio.03339-19-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/863522b89759/mBio.03339-19-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/69c2f4e9d5a4/mBio.03339-19-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/9e352e8c80c1/mBio.03339-19-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/cae7c679f246/mBio.03339-19-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/863522b89759/mBio.03339-19-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/69c2f4e9d5a4/mBio.03339-19-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b862/7018647/9e352e8c80c1/mBio.03339-19-f0004.jpg

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