Metagenomic surveillance of bacteriophages, phage-like elements and intestinal VLPs
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB33536 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 205_2M.Spades3_contigs_larger40kb.fa.gz | Other | |||
| ERR3440511_1.fastq.gz | Fastqsanger.gz | |||
| ERR3440511_2.fastq.gz | Fastqsanger.gz | |||
| ERR3440512_1.fastq.gz | Fastqsanger.gz | |||
| ERR3440512_2.fastq.gz | Fastqsanger.gz |
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Project description:Virulent bacteriophages (or phages) are viruses that specifically infect and lyse a bacterial host. When multiple phages co-infect a bacterial host, the extent of lysis, dynamics of bacteria-phage and phage-phage interactions are expected to vary. The objective of this study is to identify the factors influencing the interaction of two virulent phages with different Pseudomonas aeruginosa growth states (planktonic, an infected epithelial cell line, and biofilm) by measuring the bacterial time-kill and individual phage replication kinetics. A single administration of phages effectively reduced P. aeruginosa viability in planktonic conditions and infected human lung cell cultures, but phage-resistant variants subsequently emerged. In static biofilms, the phage combination displayed initial inhibition of biofilm dispersal, but sustained control was achieved only by combining phages and meropenem antibiotic. In contrast, adherent biofilms showed tolerance to phage and/or meropenem, suggesting a spatiotemporal variation in the phage-bacterial interaction. The kinetics of adsorption of each phage to P. aeruginosa during single- or co-administration were comparable. However, the phage with the shorter lysis time depleted bacterial resources early and selected a specific nucleotide polymorphism that conferred a competitive disadvantage and cross-resistance to the second phage. The extent and strength of this phage-phage competition and genetic loci conferring phage resistance, are, however, P. aeruginosa genotype dependent. Nevertheless, adding phages sequentially resulted in their unimpeded replication with no significant increase in bacterial host lysis. These results highlight the interrelatedness of phage-phage competition, phage resistance and specific bacterial growth state (planktonic/biofilm) in shaping the interplay among P. aeruginosa and virulent phages.
2024-07-17 | GSE271537 | GEO
Project description:Bacteriophage (phage) therapy is a promising alternative to antibiotics, yet phage-induced immune responses can affect treatment efficacy. However, current methods for assessing phage immunogenicity are limited, hindering the development of safer, more effective therapies. Here, we introduce the Bacteriophage Risk Index (BRI), a novel metric that quantifies phage immunogenic potential based on CpG dinucleotide frequency, motif spacing, and sequence context, key factors influencing Toll-like receptor 9 (TLR9) activation. Applying the BRI to 7,011 phage genomes, we classified them into five risk tiers, revealing substantial immunogenic variability, even among phages targeting the same bacterial host. BRI scores correlated with immune responses in human lung epithelial cells, validating its predictive power. Experimental testing further confirmed this, as exposure of lung epithelial cells to two phages from distinct risk tiers showed that the high-risk phage (Category 4) induced a strong pro-inflammatory response, upregulating CXCL1, CXCL8, IRF7, and TNFAIP3, while the low-risk phage (Category 2) triggered minimal immune activation with limited cytokine expression. These findings confirm that higher BRI scores predict stronger immune responses, providing a robust tool for evaluating phage immunogenicity. By enabling the selection of phages with lower immunogenic potential, the BRI enhances the safety and efficacy of phage therapy while offering a standardized framework for regulatory agencies, clinical researchers, and biologic drug development, with applications extending beyond phage therapy to other immunogenic biologics.
2025-06-16 | GSE293045 | GEO
Project description:Purified phage was used to prevent tumor growth in a mouse model of bacteria aggravated-colorectal cancer. Composite E. coli phage or vehicle control was added to the drinking water of specific pathogen free (SPF) APCmin mice and animals were colonized with E.coli NC101. APCmin mice displayed no overall difference in the number of tumors that formed within the small intestine, however colonization with E. coli NC101 accelerated the growth of tumors resulting in a significant increase in large tumor formation. Importantly, bacteriophage treatment of AIEC colonized APCmin animals significantly reduced E. coli colonization.
2019-03-01 | GSE124123 | GEO
Project description:RNA-sequencing was preformed from RNA isolated from bacteria infected with the bacteriophage. In order to reveal the phage-host interactions between φR1-37 and Yersinia enterocolitica throughout the phage infection cycle, both the transcriptomes were scrutinized during all the stages of infection.
2016-01-22 | GSE77068 | GEO
Project description:Staphylococcus phage 812, strain K1/420, is a broad-acting bacteriophage infecting S. aureus. Phage 812 belongs to the family Herelleviridae and is closely related to kayviruses. We conducted a structural study of the viral particle of phage 812 before and after genome ejection. We characterized the protein components forming the particle and described the changes in their structural arrangement that govern genome anchoring, gating, and release.
2026-01-19 | PXD071586 | Pride
Project description:Bacteriophage (phage) are viruses that can kill bacteria, but also mediate gene transfer for bacterial evolution. The telomere phages are a curious form using telomere-like structures to replicate their genomes as linear extrachromosomal elements. Here we find that telomere phages are widely distributed in bacteria, being highly prevalent in Klebsiella species. We established a model system to investigate telomere phage biology and find only a small set of phage proteins are expressed in phage-host cells, including a toxin – telocin - that kills other Klebsiella strains. We identify and validate other telocins in the genomes of other, widespread Klebsiella telomere phages. Thus, telomere phages are widespread elements encoding diverse antibacterial weapons and we discuss the prospect of using telocins for precision editing of microbial populations.
2025-05-07 | PXD058604 | Pride
Project description:An important lesson from the war on pathogenic bacteria has been the need to understand the physiological responses and evolution of natural microbial communities. Bacterial populations in the environment are generally forming biofilms subject to some level of phage predation. These multicellular communities are notoriously resistant to antimicrobials and, consequently, very difficult to eradicate. This has sparked the search for new therapeutic alternatives, including phage therapy. This study demonstrates that S. aureus biofilms formed in the presence of a non-lethal dose of phage phiIPLA-RODI exhibit a unique physiological state that could potentially benefit both the host and the predator. Thus, biofilms formed under phage pressure are thicker and have a greater DNA content. Also, the virus-infected biofilm displayed major transcriptional differences compared to an untreated control. Significantly, RNA-seq data revealed activation of the stringent response, which could slow down the advance of the bacteriophage within the biofilm. The end result would be an equilibrium that would help bacterial cells to withstand environmental challenges, while maintaining a reservoir of sensitive bacterial cells available to the phage upon reactivation of the dormant carrier population.
2017-01-20 | GSE87706 | GEO
Project description:The basic biology of bacteriophage–host interactions has attracted increasing attention due to a renewed interest in the therapeutic potential of bacteriophages. In addition, knowledge of the host pathways inhibited by phage may provide clues to novel drug targets. However, the effect of phage on bacterial gene expression and metabolism is still poorly understood. In this study, we tracked phage–host interactions by combining transcriptomic and metabolomic analyses in Pseudomonas aeruginosa infected with a lytic bacteriophage, PaP1. Compared with the uninfected host, 7.1% (399/5655) of the genes of the phage-infected host were differentially expressed genes (DEGs); of those, 354 DEGs were downregulated at the late infection phase. Many of the downregulated DEGs were found in amino acid and energy metabolism pathways. Using metabolomics approach, we then analyzed the changes in metabolite levels in the PaP1-infected host compared to un-infected controls. Thymidine was significantly increased in the host after PaP1 infection, results that were further supported by increased expression of a PaP1-encoded thymidylate synthase gene. Furthermore, the intracellular betaine concentration was drastically reduced, whereas choline increased, presumably due to downregulation of the choline–glycine betaine pathway. Interestingly, the choline–glycine betaine pathway is a potential antimicrobial target; previous studies have shown that betB inhibition results in the depletion of betaine and the accumulation of betaine aldehyde, the combination of which is toxic to P. aeruginosa. These results present a detailed description of an example of phage-directed metabolism in P. aeruginosa. Both phage-encoded auxiliary metabolic genes and phage-directed host gene expression may contribute to the metabolic changes observed in the host.
2018-05-03 | MTBLS431 | MetaboLights
Project description:Bacteriophage P1 is one of the most commonly studied phages in molecular biology, and P1vir, its virulent derivative, has been widely used in almost every biotechnological laboratory as a useful genetic tool. Phage development depends on many host proteins and the cellular physiological state. In many cases, metabolic control is assessed by efficient and energy-saving riboregulation, and one of the major cellular hub of the global RNA regulation is the Hfq protein. Despite the fact that this factor was discovered as host factor necessary for Qβ bacteriophage replication, the role of Hfq in phage biology has not been extensively studied. We have found that deletion of the hfq gene resulted in impaired development of P1vir, suggesting its important role, but not indispensability, in the phage biology. We demonstrate global changes in the host-virus transcriptome during the infection. We have found that at different times after infection of the wild type strain (10 and 20 min), numerous hosts genes have been downregulated. On the other hand, in the Δhfq mutant, relatively small number of genes has been downregulated. Furthermore, numerous viral genes have been downregulated in the Δhfq mutant, comparing to the wild-type cells. Our results demonstrate that deficiency in global RNA regulation severely affects phage P1vir development. Thus, observed impaired P1vir development can be explained by abolition of proper cell re-programming during infection and/or impaired phage gene expression. The Hfq protein, as a global RNA hub, occurs in Escherichia coli and its homologues are present in other bacteria and archeons. Therefore, we anticipate that our results put new light on Hfq as a global phage regulator.
2025-12-31 | GSE262812 | GEO