Evidence map›Paper›PMID 24824286›Full record

ArticleHeredity2014

On the definition and utilization of heritable variation among hosts in reproduction ratio R0 for infectious diseases.

M T Anche, M C M de Jong, P Bijma

Open access · bronzeAbstract read
In one paragraph

Article in Heredity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Age-structured next generation matrix and RInfectious Disease Modelling · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Why DoesFrontiers in immunology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. The Price equation as a bridge between animal breeding and evolutionary biology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  13. The economic value of RGenetics, selection, evolution : GSE · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Derivation of the economic value of RGenetics, selection, evolution : GSE · 2018
    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

3 authors at 1 institution in 1 country.

M T Anche1] Animal Breeding and Genomics Centre, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, Wageningen, The Netherlands [2] Quantitative Veterinary Epidemiology Group, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, Wageningen, The Netherlands.
M C M de JongQuantitative Veterinary Epidemiology Group, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, Wageningen, The Netherlands.
P BijmaAnimal Breeding and Genomics Centre, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, Wageningen, The Netherlands.
Wageningen University & Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infectious diseases have a major role in evolution by natural selection and pose a worldwide concern in livestock. Understanding quantitative genetics of infectious diseases, therefore, is essential both for understanding the consequences of natural selection and for designing artificial selection schemes in agriculture. The basic reproduction ratio, R0, is the key parameter determining risk and severity of infectious diseases. Genetic improvement for control of infectious diseases in host populations should therefore aim at reducing R0. This requires definitions of breeding value and heritable variation for R0, and understanding of mechanisms determining response to selection. This is challenging, as R0 is an emergent trait arising from interactions among individuals in the population. Here we show how to define breeding value and heritable variation for R0 for genetically heterogeneous host populations. Furthermore, we identify mechanisms determining utilization of heritable variation for R0. Using indirect genetic effects, next-generation matrices and a SIR (Susceptible, Infected and Recovered) model, we show that an individual's breeding value for R0 is a function of its own allele frequencies for susceptibility and infectivity and of population average susceptibility and infectivity. When interacting individuals are unrelated, selection for individual disease status captures heritable variation in susceptibility only, yielding limited response in R0. With related individuals, however, there is a secondary selection process, which also captures heritable variation in infectivity and additional variation in susceptibility, yielding substantially greater response. This shows that genetic variation in susceptibility represents an indirect genetic effect. As a consequence, response in R0 increased substantially when interacting individuals were genetically related.

Indexed as

Genetic VariationReproductionDiseaseDisease SusceptibilityGenetics, PopulationHumansInfectionsModels, Genetic

Identifiers

PMID24824286
PMCPMC4181063
OpenAlexW2089453318

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.