珊瑚礁上宿主特异性病毒捕食网络

Natascha S Varona, Poppy J Hesketh-Best, Felipe H Coutinho, Alexandra K Stiffler, Bailey A Wallace, Sofia L Garcia, Yun Scholten, Andreas F Haas, Mark Little, Mark Vermeij, Antoni Luque, Cynthia Silveira
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摘要

病毒感染是海洋微生物群落聚集和生物地球化学循环的主要调节因子。在珊瑚礁中,病毒裂解控制了对珊瑚健康有害的细菌过度生长。然而,方法上的限制阻碍了病毒宿主的识别和它们相互作用频率的量化。在这里,我们通过将直接显微镜计数与通过邻近结扎、噬菌体整合和CRISPR间隔物获得的病毒-宿主联系结合起来,在cura寡营养珊瑚礁水域重建了丰度分辨率的病毒-细菌相互作用网络。这个由3,013个单独链接(97个独特的物种水平相互作用)组成的网络揭示了游离病毒颗粒的丰度与宿主丰度和病毒产量的弱相关性,正如细胞相关的病毒与宿主比率所表明的那样。具有最高的游离病毒和细胞相关病毒与宿主比率的病毒,在这里被解释为高产病毒,与属于γ变形菌门、拟杆菌门和plantomyctia的中低丰度宿主形成联系。相反,低产量病毒与丰富的α变形菌和γ变形菌相互作用。这些发现强调了病毒丰度和生产之间的脱钩,并确定了潜在的活性病毒。我们认为,不同的衰减率和爆发大小可以解释游离病毒丰度和生产之间的脱钩,并且溶原性感染在高丰度宿主的生态中起着重要作用。
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Host-specific viral predation network on coral reefs
Viral infections are major modulators of marine microbial community assembly and biogeochemical cycling. In coral reefs, viral lysis controls bacterial overgrowth that is detrimental to coral health. However, methodological limitations have prevented the identification of viral hosts and quantification of their interaction frequencies. Here, we reconstructed an abundance-resolved virus-bacteria interaction network in the oligotrophic coral reef waters of Curaçao by integrating direct microscopy counts with virus-host links obtained from proximity-ligation, prophage integration, and CRISPR spacers. This network of 3,013 individual links (97 unique species-level interactions) revealed that the abundance of free viral particles was weakly related to host abundance and viral production, as indicated by the cell-associated virus-to-host ratio. The viruses with the highest free and cell-associated virus-to-host ratio, interpreted here as highly productive viruses, formed links with intermediate-to-low abundance hosts belonging to Gammaproteobacteria, Bacteroidia, and Planctomycetia. In contrast, low-production viruses interacted with abundant members of Alphaproteobacteria and Gammaproteobacteria enriched in prophages. These findings highlight the decoupling between viral abundance and production and identify potentially active viruses. We propose that differential decay rates and burst sizes may explain the decoupling between free viral abundance and production and that lysogenic infections play an important role in the ecology of high-abundance hosts.
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