Evidence map›Paper›PMID 25519990›Full record

ArticleJournal of the Royal Society, Interface2015

Minimal within-host dengue models highlight the specific roles of the immune response in primary and secondary dengue infections.

Rotem Ben-Shachar, Katia Koelle

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Identifiability investigation of within-host models of acute virus infection.Mathematical biosciences and engineering : MBE · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Boosting can explain patterns of fluctuations of ratios of inapparent to symptomatic dengue virus infections.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

2 authors at 2 institutions in 1 country.

Rotem Ben-ShacharProgram in Computational Biology and Bioinformatics, Duke University, Durham, NC, USA rotem.ben.shachar@duke.edu.
Katia KoelleDepartment of Biology, Duke University, Durham, NC, USA Fogarty International Center, National Institute of Health, Bethesda, MD, USA.
Duke University · USFogarty International Center · US

Funding

Computational Biology and Bioinformatics Training ProgramT32GM071340 · NIGMS · DUKE UNIVERSITY · PI MAGWENE, PAUL MITAARI · 2005 to 2020
$3.3M
NIGMS NIH HHS T32 GM071340
6 · The paper itself

Abstract

In recent years, the within-host viral dynamics of dengue infections have been increasingly characterized, and the relationship between aspects of these dynamics and the manifestation of severe disease has been increasingly probed. Despite this progress, there are few mathematical models of within-host dengue dynamics, and the ones that exist focus primarily on the general role of immune cells in the clearance of infected cells, while neglecting other components of the immune response in limiting viraemia. Here, by considering a suite of mathematical within-host dengue models of increasing complexity, we aim to isolate the critical components of the innate and the adaptive immune response that suffice in the reproduction of several well-characterized features of primary and secondary dengue infections. By building up from a simple target cell limited model, we show that only the innate immune response is needed to recover the characteristic features of a primary symptomatic dengue infection, while a higher rate of viral infectivity (indicative of antibody-dependent enhancement) and infected cell clearance by T cells are further needed to recover the characteristic features of a secondary dengue infection. We show that these minimal models can reproduce the increased risk of disease associated with secondary heterologous infections that arises as a result of a cytokine storm, and, further, that they are consistent with virological indicators that predict the onset of severe disease, such as the magnitude of peak viraemia, time to peak viral load, and viral clearance rate. Finally, we show that the effectiveness of these virological indicators to predict the onset of severe disease depends on the contribution of T cells in fuelling the cytokine storm.

Indexed as

Models, ImmunologicalAnimalsDengueDengue VirusHost-Pathogen InteractionsHumansViremiacytokine stormdenguedisease severityimmune responsemathematical modelviral dynamics

Identifiers

PMID25519990
PMCPMC4305404
OpenAlexW2165676801

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.