ArticleWorld journal of microbiology & biotechnology2026
Construction and characterization of a chimeric Salmonella phage P6-UPF2 via homologous replacement of the phage P6 tail spike protein Gp9.
Article in World journal of microbiology & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
With over 2,600 Salmonella serotypes identified, no single natural or existing bacteriophage can cover this diversity, making customized phages a promising strategy for precise control. In this study, the previously characterized phage P6 served as the recipient, and the broad-spectrum phage UPF_BP1 (94.91% nucleotide identity with P6) served as the donor. Two fragments (b1 and b2) from the donor's tail spike protein gene were individually recombined into the Gp9 locus of P6, generating two chimeric phages: P6-UPF1 and P6-UPF2. Host range analysis showed that P6-UPF1 exhibited no alteration in host spectrum against the bacterial strains tested, whereas P6-UPF2 retained activity against S. Enteritidis, S. Typhimurium, and S. Bovismorbificans, and gained activity against S. Muenster and S. Newlands, with preliminary evidence of genetic stability. Competitive adsorption inhibition assays showed that UPF-b2 significantly suppressed the adsorption of P6-UPF2 to S. Typhimurium, S. Muenster, and S. Newlands (P < 0.001), whereas P6-b1 significantly inhibited the adsorption of P6-UPF2 to S. Enteritidis (P < 0.001). The results identify, for the first time, the UPF-b2 and P6-b1 fragments within the Gp9 tail spike protein of P22-like phages as host range determinants for S. Typhimurium, S. Muenster, S. Newlands, and S. Enteritidis, respectively. Biological characterization indicated that P6-UPF2 exhibited an optimal multiplicity of infection of 0.1, a latent period of 10 min, a burst period of 90 min, and a burst size of up to 10
Indexed as
Identifiers
42911508What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.