Department of Biology, San Diego State University, 5500 Campanile Dr, San Diego, CA, 92182, USA.
Viral Information Institute, San Diego State University, 5500 Campanile Dr, San Diego, CA, 92182, USA.
BMC Genomics. 2020 Feb 5;21(1):126. doi: 10.1186/s12864-020-6523-2.
Bacteriophages encode genes that modify bacterial functions during infection. The acquisition of phage-encoded virulence genes is a major mechanism for the rise of bacterial pathogens. In coral reefs, high bacterial density and lysogeny has been proposed to exacerbate reef decline through the transfer of phage-encoded virulence genes. However, the functions and distribution of these genes in phage virions on the reef remain unknown.
Here, over 28,000 assembled viral genomes from the free viral community in Atlantic and Pacific Ocean coral reefs were queried against a curated database of virulence genes. The diversity of virulence genes encoded in the viral genomes was tested for relationships with host taxonomy and bacterial density in the environment. These analyses showed that bacterial density predicted the profile of virulence genes encoded by phages. The Shannon diversity of virulence-encoding phages was negatively related with bacterial density, leading to dominance of fewer genes at high bacterial abundances. A statistical learning analysis showed that reefs with high microbial density were enriched in viruses encoding genes enabling bacterial recognition and invasion of metazoan epithelium. Over 60% of phages could not have their hosts identified due to limitations of host prediction tools; for those which hosts were identified, host taxonomy was not an indicator of the presence of virulence genes.
This study described bacterial virulence factors encoded in the genomes of bacteriophages at the community level. The results showed that the increase in microbial densities that occurs during coral reef degradation is associated with a change in the genomic repertoire of bacteriophages, specifically in the diversity and distribution of bacterial virulence genes. This suggests that phages are implicated in the rise of pathogens in disturbed marine ecosystems.
噬菌体编码的基因在感染过程中会改变细菌的功能。噬菌体编码的毒力基因的获得是细菌病原体兴起的主要机制。在珊瑚礁中，高细菌密度和溶原性被认为通过噬菌体编码的毒力基因的转移加剧了珊瑚礁的衰退。然而，这些基因在珊瑚礁上噬菌体病毒粒子中的功能和分布仍然未知。
在这里，对大西洋和太平洋珊瑚礁中自由病毒群中超过 28000 个组装的病毒基因组进行了查询，以对抗经过精心整理的毒力基因数据库。测试了病毒基因组中编码的毒力基因的多样性与宿主分类和环境中细菌密度的关系。这些分析表明，细菌密度预测了噬菌体编码的毒力基因的特征。编码毒力的噬菌体的 Shannon 多样性与细菌密度呈负相关，导致在高细菌丰度下，更少的基因占主导地位。统计学习分析表明，微生物密度高的珊瑚礁富含能够使细菌识别和入侵后生动物上皮的病毒，编码这些基因。由于宿主预测工具的限制，超过 60%的噬菌体无法确定其宿主；对于那些可以确定宿主的噬菌体，宿主分类法并不是毒力基因存在的指标。
本研究在群落水平上描述了噬菌体基因组中编码的细菌毒力因子。结果表明，在珊瑚礁退化过程中微生物密度的增加与噬菌体基因组谱的变化有关，特别是在细菌毒力基因的多样性和分布方面。这表明噬菌体可能与受干扰的海洋生态系统中病原体的兴起有关。
