Evidence map›Paper›PMID 23468631›Full record

ArticlePLoS pathogens2013

Phylodynamic analysis of the emergence and epidemiological impact of transmissible defective dengue viruses.

Ruian Ke, John Aaskov, Edward C Holmes, James O Lloyd-Smith

Open access · goldAbstract 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
0.3field-weighted citation impact, top 32% 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

31 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Spatio-temporal modelling ofbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Antigenic characterization of influenza and SARS-CoV-2 viruses.Analytical and bioanalytical chemistry · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. RNA (New York, N.Y.) · 2018
    Article
  16. Review
  17. Understanding dengue virus evolution to support epidemic surveillance and counter-measure development.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2018
    Review
  18. Review
  19. Article
  20. 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

4 authors at 4 institutions in 2 countries.

Ruian KeDepartment of Ecology and Evolutionary Biology, University of California, Los Angeles, California, United States of America. ruian@ucla.edu
John Aaskov
Edward C Holmes
James O Lloyd-Smith
National Institutes of Health · USQueensland University of Technology · AUUniversity of California, Los Angeles · USUniversity of Sydney · AU

Funding

The Evolutionary and Biological Bases of Host Switching in VirusesR01GM080533 · NIGMS · PENNSYLVANIA STATE UNIVERSITY, THE · PI PARRISH, COLIN R. · 2007 to 2019
$4.1M
Fitness and Virulence of Dengue Virus in the Context of Changing Host ImmunityR01GM087405 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI HARRIS, EVA · 2009 to 2012
$1.2M
NIGMS NIH HHS 5R01GM087405-03NIGMS NIH HHS R01 GM080533NIGMS NIH HHS R01GM080533-06NIGMS NIH HHS R01 GM087405
6 · The paper itself

Abstract

Intra-host sequence data from RNA viruses have revealed the ubiquity of defective viruses in natural viral populations, sometimes at surprisingly high frequency. Although defective viruses have long been known to laboratory virologists, their relevance in clinical and epidemiological settings has not been established. The discovery of long-term transmission of a defective lineage of dengue virus type 1 (DENV-1) in Myanmar, first seen in 2001, raised important questions about the emergence of transmissible defective viruses and their role in viral epidemiology. By combining phylogenetic analyses and dynamical modeling, we investigate how evolutionary and ecological processes at the intra-host and inter-host scales shaped the emergence and spread of the defective DENV-1 lineage. We show that this lineage of defective viruses emerged between June 1998 and February 2001, and that the defective virus was transmitted primarily through co-transmission with the functional virus to uninfected individuals. We provide evidence that, surprisingly, this co-transmission route has a higher transmission potential than transmission of functional dengue viruses alone. Consequently, we predict that the defective lineage should increase overall incidence of dengue infection, which could account for the historically high dengue incidence reported in Myanmar in 2001-2002. Our results show the unappreciated potential for defective viruses to impact the epidemiology of human pathogens, possibly by modifying the virulence-transmissibility trade-off, or to emerge as circulating infections in their own right. They also demonstrate that interactions between viral variants, such as complementation, can open new pathways to viral emergence.

Indexed as

Disease OutbreaksHost-Pathogen InteractionsDefective VirusesDengueDengue VirusEndemic DiseasesHumansMolecular EpidemiologyMyanmarPhylogeographySpecies Specificity

Identifiers

PMID23468631
PMCPMC3585136
OpenAlexW1595241928

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.