Plymouth Marine Laboratory, Prospect Place, The Hoe, Plymouth, PL1 3DH, UK.
University of Exeter, Geoffrey Pope Building, Stocker Road, Exeter, EX4 4QD, UK.
Virol J. 2019 Feb 1;16(1):15. doi: 10.1186/s12985-019-1120-1.
Microbial communities living in the oceans are major drivers of global biogeochemical cycles. With nutrients limited across vast swathes of the ocean, marine microbes eke out a living under constant assault from predatory viruses. Viral concentrations exceed those of their bacterial prey by an order of magnitude in surface water, making these obligate parasites the most abundant biological entities in the ocean. Like the pirates of the 17th and 18th centuries that hounded ships plying major trade and exploration routes, viruses have evolved mechanisms to hijack microbial cells and repurpose their cargo and indeed the vessels themselves to maximise viral propagation. Phenotypic reconfiguration of the host is often achieved through Auxiliary Metabolic Genes - genes originally derived from host genomes but maintained and adapted in viral genomes to redirect energy and substrates towards viral synthesis. In this review, we critically evaluate the literature describing the mechanisms used by bacteriophages to reconfigure host metabolism and to plunder intracellular resources to optimise viral production. We also highlight the mechanisms used when, in challenging environments, a 'batten down the hatches' strategy supersedes that of 'plunder and pillage'. Here, the infecting virus increases host fitness through phenotypic augmentation in order to ride out the metaphorical storm, with a concomitant impact on host substrate uptake and metabolism, and ultimately, their interactions with their wider microbial community. Thus, the traditional view of the virus-host relationship as predator and prey does not fully characterise the variety or significance of the interactions observed. Recent advances in viral metagenomics have provided a tantalising glimpse of novel mechanisms of viral metabolic reprogramming in global oceans. Incorporation of these new findings into global biogeochemical models requires experimental evidence from model systems and major improvements in our ability to accurately predict protein function from sequence data.
海洋中的微生物群落是全球生物地球化学循环的主要驱动因素。由于营养物质在海洋的大片区域受到限制,海洋微生物在不断受到掠食性病毒的攻击下艰难求生。在地表水层中,病毒的浓度比其细菌猎物高出一个数量级,使得这些专性寄生虫成为海洋中最丰富的生物实体。就像 17 世纪和 18 世纪在主要贸易和探险航线上骚扰船只的海盗一样,病毒已经进化出了劫持微生物细胞并重新利用其货物甚至是宿主本身的机制,以最大限度地提高病毒的繁殖。宿主的表型重构通常是通过辅助代谢基因实现的——这些基因最初来自宿主基因组,但在病毒基因组中被维持和适应,以将能量和底物重新导向病毒合成。在这篇综述中,我们批判性地评估了描述噬菌体重新配置宿主代谢和掠夺细胞内资源以优化病毒产生的机制的文献。我们还强调了在具有挑战性的环境中,“关紧舱门”策略取代“掠夺和掠夺”策略时所使用的机制。在这种情况下,感染病毒通过表型增强来提高宿主的适应性,以度过隐喻中的风暴,这对宿主底物摄取和代谢产生了相应的影响,并最终影响了它们与更广泛的微生物群落的相互作用。因此,病毒-宿主关系作为捕食者和猎物的传统观点并不能完全描述所观察到的相互作用的多样性或重要性。病毒宏基因组学的最新进展为全球海洋中病毒代谢重编程的新机制提供了诱人的一瞥。将这些新发现纳入全球生物地球化学模型需要来自模型系统的实验证据,并需要大大提高我们从序列数据准确预测蛋白质功能的能力。