原噬菌体通过其改变致病细菌性状的能力具有重大的临床意义。对于幽门螺杆菌（一种与胃癌有因果关系的广泛存在的细菌）的生态、进化、适应过程和致病性中的原噬菌体作用的了解有限。推断确切的原噬菌体基因组位置和完整性需要完整的基因组。国际幽门螺杆菌基因组计划 (HpGP) 数据集包含 1011 个幽门螺杆菌完整临床基因组，富含表观遗传学数据。我们彻底评估了 HpGP 数据集中的幽门螺杆菌原噬菌体基因组内容。我们通过系统发育和全基因组分析研究了种群进化动态。此外，我们还确定了基因组重排并评估了原噬菌体的存在对细菌基因破坏和甲基化组的影响。我们发现 29.5% (298) 的 HpGP 基因组含有原噬菌体，其中只有 32.2% (96) 是完整的，从而最大限度地减少了原噬菌体携带的负担。幽门螺杆菌原噬菌体序列的流行率因地理位置和血统而异，但不因人类宿主的疾病状态而异。原噬菌体插入偶尔会导致基因破坏，从而改变整体细菌表观基因组。基因功能预测使得第一个幽门螺杆菌溶原裂解循环调节模型得以开发。我们已经揭示了新的前噬菌体失活机制，该机制似乎是通过基因组重排、与其他移动元件合并以及假基因积累而发生的。我们的分析为幽门螺杆菌原噬菌体生物学和基因组学提供了一个全面的框架，为溶源调节和细菌对原噬菌体的适应提供了见解。

Prophages can have major clinical implications through their ability to change pathogenic bacterial traits. There is limited understanding of the prophage role in ecological, evolutionary, adaptive processes and pathogenicity of Helicobacter pylori, a widespread bacterium causally associated with gastric cancer. Inferring the exact prophage genomic location and completeness requires complete genomes. The international Helicobacter pylori Genome Project (HpGP) dataset comprises 1011 H. pylori complete clinical genomes enriched with epigenetic data. We thoroughly evaluated the H. pylori prophage genomic content in the HpGP dataset. We investigated population evolutionary dynamics through phylogenetic and pangenome analyses. Additionally, we identified genome rearrangements and assessed the impact of prophage presence on bacterial gene disruption and methylome. We found that 29.5% (298) of the HpGP genomes contain prophages, of which only 32.2% (96) were complete, minimizing the burden of prophage carriage. The prevalence of H. pylori prophage sequences was variable by geography and ancestry, but not by disease status of the human host. Prophage insertion occasionally results in gene disruption that can change the global bacterial epigenome. Gene function prediction allowed the development of the first model for lysogenic-lytic cycle regulation in H. pylori. We have disclosed new prophage inactivation mechanisms that appear to occur by genome rearrangement, merger with other mobile elements, and pseudogene accumulation. Our analysis provides a comprehensive framework for H. pylori prophage biological and genomics, offering insights into lysogeny regulation and bacterial adaptation to prophages.