Bacteriophages from human skin infecting coagulase-negative Staphylococcus: diversity, novel species and host resistance

Bacteriophages from human skin infecting coagulase-negative Staphylococcus: diversity, novel species and host resistance
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来自人类皮肤的噬菌体感染凝固酶阴性葡萄球菌:多样性、新物种和宿主抗性

DOI:
10.1101/2023.11.07.565964
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发表时间:
2023
期刊:
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影响因子:
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通讯作者:
Alsaadi S
Alsaadi S
中科院分区:
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文献类型:
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作者:
Alsaadi S

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人体皮肤微生物组包括不同的种群,在身体部位和个体之间存在时间性差异。病毒体是皮肤微生物组中研究较少的组成部分,需要对噬菌体进行研究,以增加对细菌群落的调节和稳定性的了解。葡萄球菌是最丰富的皮肤殖民者之一,与健康和疾病有关,但感染皮肤上最丰富物种的噬菌体的研究较少。在这里,我们报道了从感染凝固酶阴性葡萄球菌(con)物种的人皮肤拭子中分离出40个噬菌体并进行基因组测序,这扩展了我们对噬菌体多样性的认识。鉴定了六个噬菌体遗传集群,其中两个集群代表新的噬菌体,其中一个我们表征并命名为Alsa噬菌体。我们发现阿尔萨噬菌体感染物种的能力更强。与其他con物种相比,被分离的噬菌体感染较少的人科动物,这表明一种未描述的噬菌体感染屏障可能部分归因于许多限制性修饰系统。葡萄球菌的广泛多样性使得进一步的研究能够确定它们对皮肤微生物组研究的贡献以及限制噬菌体感染的机制。
The human skin microbiome comprises diverse populations that differ temporally between body sites and individuals. The virome is a less studied component of the skin microbiome and the study of bacteriophages is required to increase knowledge of the modulation and stability of bacterial communities.Staphylococcusspecies are among the most abundant colonisers of skin and are associated with both health and disease yet the bacteriophages infecting the most abundant species on skin are less well studied. Here, we report the isolation and genome sequencing of 40 bacteriophages from human skin swabs that infect coagulase-negativeStaphylococcus(CoNS) species, which extends our knowledge of phage diversity. Six genetic clusters of phages were identified with two clusters representing novel phages, one of which we characterise and name Alsa phage. We identified that Alsa phages have a greater ability to infect the speciesS. hoministhat was otherwise infected less than other CoNS species by the isolated phages, indicating an undescribed barrier to phage infection that could be in part due to numerous restriction-modification systems. The extended diversity ofStaphylococcusphages here enables further research to define their contribution to skin microbiome research and the mechanisms that limit phage infection.