Evidence map›Paper›PMID 33054713›Full record

ReviewGenetics, selection, evolution : GSE2020

Why breed disease-resilient livestock, and how?

Pieter W Knap, Andrea Doeschl-Wilson

Open access · goldAbstract readReview
In one paragraph

Review in Genetics, selection, evolution : GSE, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
20.7field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 166 citations in OpenAlex.

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  20. Genome-Wide Association Study of Immune Indices in Yaks.Animals : an open access journal from MDPI · 2025
    Article

2 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

2 authors at 2 institutions in 3 countries.

Pieter W KnapGenus-PIC, 24837, Schleswig, Germany. Pieter.Knap@genusplc.com.ORCID http://orcid.org/0000-0001-7765-7842
Andrea Doeschl-WilsonThe Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush Estate, Edinburgh, EH25 9RG, Scotland, UK.
Gene Therapy Laboratory · FRRoslin Institute · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/D/20002172Biotechnology and Biological Sciences Research Council BBS/E/D/30002275Biotechnology and Biological Sciences Research Council BB/T004401/1Horizon 2020 Framework Programme 772787
6 · The paper itself

Abstract

backgroundFighting and controlling epidemic and endemic diseases represents a considerable cost to livestock production. Much research is dedicated to breeding disease resilient livestock, but this is not yet a common objective in practical breeding programs. In this paper, we investigate how future breeding programs may benefit from recent research on disease resilience. MAIN BODY: We define disease resilience in terms of its component traits resistance (R: the ability of a host animal to limit within-host pathogen load (PL)) and tolerance (T: the ability of an infected host to limit the damage caused by a given PL), and model the host's production performance as a reaction norm on PL, depending on R and T. Based on this, we derive equations for the economic values of resilience and its component traits. A case study on porcine respiratory and reproductive syndrome (PRRS) in pigs illustrates that the economic value of increasing production in infectious conditions through selection for R and T can be more than three times higher than by selection for production in disease-free conditions. Although this reaction norm model of resilience is helpful for quantifying its relationship to its component traits, its parameters are difficult and expensive to quantify. We consider the consequences of ignoring R and T in breeding programs that measure resilience as production in infectious conditions with unknown PL-particularly, the risk that the genetic correlation between R and T is unfavourable (antagonistic) and that a trade-off between them neutralizes the resilience improvement. We describe four approaches to avoid such antagonisms: (1) by producing sufficient PL records to estimate this correlation and check for antagonisms-if found, continue routine PL recording, and if not found, shift to cheaper proxies for PL; (2) by selection on quantitative trait loci (QTL) known to influence both R and T in favourable ways; (3) by rapidly modifying towards near-complete resistance or tolerance, (4) by re-defining resilience as the animal's capacity to resist (or recover from) the perturbation caused by an infection, measured as temporal deviations of production traits in within-host longitudinal data series.

conclusionsAll four alternatives offer promising options for genetic improvement of disease resilience, and most rely on technological and methodological developments and innovation in automated data generation.

Indexed as

Disease ResistanceAnimalsBreedingGenomicsLivestockQuantitative Trait, Heritable

Identifiers

PMID33054713
PMCPMC7557066
OpenAlexW3092952078

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.