Evidence map›Paper›PMID 23555251›Full record

ArticlePLoS pathogens2013

Kinetics of coinfection with influenza A virus and Streptococcus pneumoniae.

Amber M Smith, Frederick R Adler, Ruy M Ribeiro, Ryan N Gutenkunst, Julie L McAuley, Jonathan A McCullers, Alan S Perelson

Abstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed
–field-weighted citation impact
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

131 citing papers in PubMed.

  1. Trial
  2. Review
  3. Influenza A Virus Coinfection AltersbioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. The temporal sequence of influenza H1N1 andFrontiers in microbiology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Observational

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

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

7 authors.

Amber M SmithDepartment of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America. amber.smith@stjude.org
Frederick R Adler
Ruy M Ribeiro
Ryan N Gutenkunst
Julie L McAuley
Jonathan A McCullers
Alan S Perelson

Funding

Modeling Viral and T Lymphocyte DynamicsR01OD011095 · OD · TRIAD NATIONAL SECURITY, LLC · PI PERELSON, ALAN S · 2012 to 2024
$5.0M
COBRE Center for Evolutionary and Theoretical ImmunologyP20GM103452 · NIGMS · UNIVERSITY OF NEW MEXICO · PI LOKER, ERIC SAMUEL · 2012 to 2013
$4.2M
Immune System Modeling/HIVR01AI028433 · NIAID · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 1990 to 2021
$3.7M
Immune System Modeling/HIVR37AI028433 · NIAID · UNIVERSITY OF CALIF-LOS ALAMOS NAT LAB · PI PERELSON, ALAN S · 2002 to 2011
$2.4M
Bacterial virulence factors contributing to virus-associated pneumoniasK25AI100946 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SMITH, AMBER M · 2012 to 2016
$425k
NIAID NIH HHS AI028433NIAID NIH HHS AI100946NIAID NIH HHS HHSN272201000055CNIAID NIH HHS K25 AI100946NIAID NIH HHS R01 AI028433NIAID NIH HHS R37 AI028433NIGMS NIH HHS P20 GM103452NIGMS NIH HHS P20-GM103452NIH HHS OD011095NIH HHS R01 OD011095
6 · The paper itself

Abstract

Secondary bacterial infections are a leading cause of illness and death during epidemic and pandemic influenza. Experimental studies suggest a lethal synergism between influenza and certain bacteria, particularly Streptococcus pneumoniae, but the precise processes involved are unclear. To address the mechanisms and determine the influences of pathogen dose and strain on disease, we infected groups of mice with either the H1N1 subtype influenza A virus A/Puerto Rico/8/34 (PR8) or a version expressing the 1918 PB1-F2 protein (PR8-PB1-F2(1918)), followed seven days later with one of two S. pneumoniae strains, type 2 D39 or type 3 A66.1. We determined that, following bacterial infection, viral titers initially rebound and then decline slowly. Bacterial titers rapidly rise to high levels and remain elevated. We used a kinetic model to explore the coupled interactions and study the dominant controlling mechanisms. We hypothesize that viral titers rebound in the presence of bacteria due to enhanced viral release from infected cells, and that bacterial titers increase due to alveolar macrophage impairment. Dynamics are affected by initial bacterial dose but not by the expression of the influenza 1918 PB1-F2 protein. Our model provides a framework to investigate pathogen interaction during coinfections and to uncover dynamical differences based on inoculum size and strain.

Indexed as

CoinfectionAnimalsFemaleInfluenza A Virus, H1N1 SubtypeKineticsLungMiceMice, Inbred BALB CModels, TheoreticalOrthomyxoviridae InfectionsPneumococcal InfectionsStreptococcus pneumoniaeTime Factors

Identifiers

PMID23555251
PMCPMC3605146

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.