Evidence map›Paper›PMID 25011108›Full record

ArticleCell host & microbe2014

Influenza promotes pneumococcal growth during coinfection by providing host sialylated substrates as a nutrient source.

Steven J Siegel, Aoife M Roche, Jeffrey N Weiser

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed
16.1field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 253 citations in OpenAlex.

  1. Trial
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  3. Trial
  4. Article
  5. Review
  6. Review
  7. Article
  8. Influenza A Virus Coinfection AltersbioRxiv : the preprint server for biology · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mechanisms of bacterial host-to-host transmission.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  18. Viruses in bronchiectasis.ERJ open research · 2025
    Review
  19. Review
  20. Article

110 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Steven J SiegelDepartment of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Aoife M RocheDepartment of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Jeffrey N WeiserDepartment of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Pediatrics, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: weiser@mail.med.upenn.edu.
University of Pennsylvania · US

Funding

ROLE OF OPACITY VARIATION IN PNEUMOCOCCAL PATHOGENESISR01AI038446 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1996 to 2019
$7.4M
Mechanisms of Pneumococcal Persistence During CarriageR37AI038446 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jeffrey Neal Weiser · 2020 to 2026
$3.8M
Early Events in Pneumococcal ColonizationR01AI105168 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2014 to 2018
$2.1M
Bacterial and host factors in pneumococcal competitionR01AI078538 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2009 to 2013
$1.9M
Inflammation promoting respiratory tract infectionF30HL119030 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI SIEGEL, STEVEN JOSEPH · 2013 to 2014
$74k
NHLBI NIH HHS F30 HL119030NHLBI NIH HHS HL119030NIAID NIH HHS AI038446NIAID NIH HHS AI078538NIAID NIH HHS AI105168NIAID NIH HHS R01 AI038446NIAID NIH HHS R01 AI078538NIAID NIH HHS R01 AI105168NIAID NIH HHS R37 AI038446
6 · The paper itself

Abstract

Much of the mortality attributed to influenza virus is due to secondary bacterial pneumonia, particularly from Streptococcus pneumoniae. However, mechanisms underlying this coinfection are incompletely understood. We find that prior influenza infection enhances pneumococcal colonization of the murine nasopharynx, which in turn promotes bacterial spread to the lungs. Influenza accelerates bacterial replication in vivo, and sialic acid, a major component of airway glycoconjugates, is identified as the host-derived metabolite that stimulates pneumococcal proliferation. Influenza infection increases sialic acid and sialylated mucin availability and enhances desialylation of host glycoconjugates. Pneumococcal genes for sialic acid catabolism are required for influenza to promote bacterial growth. Decreasing sialic acid availability in vivo by genetic deletion of the major airway mucin Muc5ac or mucolytic treatment limits influenza-induced pneumococcal replication. Our findings suggest that higher rates of disease during coinfection could stem from influenza-provided sialic acid, which increases pneumococcal proliferation, colonization, and aspiration.

Indexed as

Microbial InteractionsAnimalsCoinfectionDisease Models, AnimalFoodLungMiceNasopharynxOrthomyxoviridaeOrthomyxoviridae InfectionsPneumonia, PneumococcalSialic AcidsStreptococcus pneumoniaeSialic Acids

Identifiers

PMID25011108
PMCPMC4096718
OpenAlexW1974945063

What OpenQuestion holds

Textmetadata
LicenceTDM
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.