Evidence map›Paper›PMID 28424056›Full record

ArticleGenetics, selection, evolution : GSE2017

Use of multi-trait and random regression models to identify genetic variation in tolerance to porcine reproductive and respiratory syndrome virus.

Graham Lough, Hamed Rashidi, Ilias Kyriazakis, Jack C M Dekkers, Andrew Hess, Melanie Hess, Nader Deeb, Antti Kause, Joan K Lunney, Raymond R R Rowland and 2 more

Abstract read
In one paragraph

Article in Genetics, selection, evolution : GSE, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Why breed disease-resilient livestock, and how?Genetics, selection, evolution : GSE · 2020
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

12 authors.

Graham LoughThe Roslin Institute & R(D)SVS, University of Edinburgh, Edinburgh, Midlothian, UK.ORCID 0000-0002-2767-9549
Hamed RashidiAnimal Breeding and Genomics Centre, Wageningen University and Research, PO Box 338, 6700 AH, Wageningen, The Netherlands.
Ilias KyriazakisSchool of Agriculture Food and Rural Development, Newcastle University, Newcastle upon Tyne, NE1 7RU, UK.
Jack C M DekkersDepartment of Animal Science, Iowa State University, Ames, IA, 50011, USA.
Andrew HessDepartment of Animal Science, Iowa State University, Ames, IA, 50011, USA.
Melanie HessDepartment of Animal Science, Iowa State University, Ames, IA, 50011, USA.
Nader DeebGenus plc, 100 Bluegrass Commons Blvd. Suite 2200, Hendersonville, TN, 37075, USA.
Antti KauseBiometrical Genetics, Natural Resources Institute Finland, 00790, Jokioinen, Finland.
Joan K LunneyAnimal Parasitic Diseases Laboratory, USDA, Beltsville, MD, 20705, USA.
Raymond R R RowlandCollege of Veterinary Medicine, Kansas State University, Manhattan, KS, 66506, USA.
Han A MulderAnimal Breeding and Genomics Centre, Wageningen University and Research, PO Box 338, 6700 AH, Wageningen, The Netherlands.
Andrea Doeschl-WilsonThe Roslin Institute & R(D)SVS, University of Edinburgh, Edinburgh, Midlothian, UK. andrea.wilson@roslin.ed.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/J004235/1Biotechnology and Biological Sciences Research Council BBS/E/D/20211554
6 · The paper itself

Abstract

backgroundA host can adopt two response strategies to infection: resistance (reduce pathogen load) and tolerance (minimize impact of infection on performance). Both strategies may be under genetic control and could thus be targeted for genetic improvement. Although there is evidence that supports a genetic basis for resistance to porcine reproductive and respiratory syndrome (PRRS), it is not known whether pigs also differ genetically in tolerance. We determined to what extent pigs that have been shown to vary genetically in resistance to PRRS also exhibit genetic variation in tolerance. Multi-trait linear mixed models and random regression sire models were fitted to PRRS Host Genetics Consortium data from 1320 weaned pigs (offspring of 54 sires) that were experimentally infected with a virulent strain of PRRS virus to obtain genetic parameter estimates for resistance and tolerance. Resistance was defined as the inverse of within-host viral load (VL) from 0 to 21 (VL

resultsMulti-trait analysis of ADG associated with either low or high VL was not indicative of genetic variation in tolerance. Similarly, random regression models for ADG

conclusionsEvidence for genetic variation in tolerance of pigs to PRRS was weak when based on data from infected piglets only. However, simulations indicated that genetic variance in tolerance may exist and could be detected if comparable data on uninfected relatives were available. In conclusion, of the two defense strategies, genetics of tolerance is more difficult to elucidate than genetics of resistance.

Indexed as

Genetic VariationModels, GeneticMultifactorial InheritanceAnimalsDisease ResistancePorcine Reproductive and Respiratory SyndromeSwineViral Load

Identifiers

PMID28424056
PMCPMC5396128

What OpenQuestion holds

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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.