Evidence map›Paper›PMID 26582495›Full record

ArticleBMC genomics2015

A genomic approach to understand interactions between Streptococcus pneumoniae and its bacteriophages.

Philippe Leprohon, Hélène Gingras, Siham Ouennane, Sylvain Moineau, Marc Ouellette

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 21% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. The applications of animal models in phage therapy: An update.Human vaccines & immunotherapeutics · 2023
    Review
  2. Article
  3. Frontiers in cellular and infection microbiology · 2021
    Article
  4. Lysogeny inMicroorganisms · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Complete Genome Sequence ofGenome announcements · 2017
    Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Philippe LeprohonCentre de recherche en Infectiologie du Centre de Recherche du CHU de Québec, Université Laval, 2705 Boul. Laurier, Québec, QC, Canada, , G1V 4G2. philippe.leprohon@crchul.ulaval.ca.
Hélène GingrasCentre de recherche en Infectiologie du Centre de Recherche du CHU de Québec, Université Laval, 2705 Boul. Laurier, Québec, QC, Canada, , G1V 4G2. helene.gingras@crchul.ulaval.ca.
Siham OuennaneDépartement de Biochimie, Microbiologie et Bio-informatique and PROTEO, Faculté des Sciences et Génie, Université Laval, Québec, QC, Canada. siham.ouennane.1@ulaval.ca.
Sylvain MoineauDépartement de Biochimie, Microbiologie et Bio-informatique and PROTEO, Faculté des Sciences et Génie, Université Laval, Québec, QC, Canada. Sylvain.Moineau@bcm.ulaval.ca.
Marc OuelletteCentre de recherche en Infectiologie du Centre de Recherche du CHU de Québec, Université Laval, 2705 Boul. Laurier, Québec, QC, Canada, , G1V 4G2. Marc.Ouellette@crchul.ulaval.ca.
Université Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBacteriophage replication depends on bacterial proteins and inactivation of genes coding for such host factors should interfere with phage infection. To gain further insights into the interactions between S. pneumoniae and its pneumophages, we characterized S. pneumoniae mutants selected for resistance to the virulent phages SOCP or Dp-1.

resultsS. pneumoniae R6-SOCP(R) and R6-DP1(R) were highly resistant to the phage used for their selection and no cross-resistance between the two phages was detected. Adsorption of SOCP to R6-SOCP(R) was partly reduced whereas no difference in Dp-1 adsorption was noted on R6-DP1(R). The replication of SOCP was completely inhibited in R6-SOCP(R) while Dp-1 was severely impaired in R6-DP1(R). Genome sequencing identified 8 and 2 genes mutated in R6-SOCP(R) and R6-DP1(R), respectively. Resistance reconstruction in phage-sensitive S. pneumoniae confirmed that mutations in a GntR-type regulator, in a glycerophosphoryl phosphodiesterase and in a Mur ligase were responsible for resistance to SOCP. The three mutations were additive to increase resistance to SOCP. In contrast, resistance to Dp-1 in R6-DP1(R) resulted from mutations in a unique gene coding for a type IV restriction endonuclease.

conclusionThe characterization of mutations conferring resistance to pneumophages highlighted that diverse host genes are involved in the replication of phages from different families.

Indexed as

GenomicsAdsorptionBacteriophagesHost-Pathogen InteractionsMutationStreptococcus pneumoniaeVirus Replication

Identifiers

PMID26582495
PMCPMC4652380
OpenAlexW2179772159

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.