scholarly journals Estimating host genetic effects on susceptibility and infectivity to infectious diseases and their contribution to response to selection

2016 ◽  
Author(s):  
M.T. Anche
Keyword(s):  
Infectious Diseases ◽  
Genetic Effects ◽  
Response To Selection ◽  
Host Genetic

scholarly journals The quantitative genetics of the endemic prevalence of infectious diseases: Indirect Genetic Effects dominate heritable variation and response to selection

2021 ◽  
Author(s):  
Piter Bijma ◽  
Andries Hulst ◽  
Mart C. M. de Jong
Keyword(s):  
Infectious Disease ◽  
Infectious Diseases ◽  
Disease Status ◽  
Host Population ◽  
Genetic Effects ◽  
Breeding Value ◽  
Response To Selection ◽  
Heritable Variation ◽  
Genetic Theory ◽  
Quantitative Genetic

AbstractPathogens have profound effects on life on earth, both in nature and agriculture. Despite the availability of well-established epidemiological theory, however, a quantitative genetic theory of the host population for the endemic prevalence of infectious diseases is almost entirely lacking. While several studies have demonstrated the relevance of the transmission dynamics of infectious diseases for heritable variation and response to selection of the host population, our current theoretical framework of quantitative genetics does not include these dynamics. As a consequence, we do not know which genetic effects of the host population determine the prevalence of an infectious disease, and have no concepts of breeding value and heritable variation for endemic prevalence.Here we propose a quantitative genetic theory for the endemic prevalence of infectious diseases. We first identify the genetic factors that determine the prevalence of an infectious disease, using an approach founded in epidemiological theory. Subsequently we investigate the population level effects of individual genetic variation on R0 and on the endemic prevalence. Next, we present expressions for the breeding value and heritable variation, for both prevalence and individual binary disease status, and show how these parameters depend on the endemic prevalence. Results show that heritable variation for endemic prevalence is substantially greater than currently believed, and increases when prevalence approaches zero, while heritability of individual disease status goes to zero. We show that response of prevalence to selection accelerates considerably when prevalence goes down, in contrast to predictions based on classical genetic models. Finally, we show that most of the heritable variation in the endemic prevalence of the infection is due to indirect genetic effects, suggestion a key role for kin-group selection both in the evolutionary history of current populations and for genetic improvement strategies in animals and plants.

scholarly journals The quantitative genetics of the prevalence of infectious diseases: hidden genetic variation due to Indirect Genetic Effects dominates heritable variation and response to selection

Genetics ◽  
2021 ◽  
Author(s):  
Piter Bijma ◽  
Andries D Hulst ◽  
Mart C M de Jong
Keyword(s):  
Genetic Variation ◽  
Infectious Diseases ◽  
Quantitative Genetics ◽  
Disease Status ◽  
Genetic Effects ◽  
Breeding Value ◽  
Response To Selection ◽  
Heritable Variation ◽  
Genetic Theory ◽  
Quantitative Genetic

Abstract Infectious diseases have profound effects on life, both in nature and agriculture. However, a quantitative genetic theory of the host population for the endemic prevalence of infectious diseases is almost entirely lacking. While several studies have demonstrated the relevance of transmission of infections for heritable variation and response to selection, current quantitative genetics ignores transmission. Thus, we lack concepts of breeding value and heritable variation for endemic prevalence, and poorly understand response of endemic prevalence to selection. Here we integrate quantitative genetics and epidemiology, and propose a quantitative genetic theory for the basic reproduction number R0 and for the endemic prevalence of an infection. We first identify the genetic factors that determine the prevalence. Subsequently we investigate the population level consequences of individual genetic variation, for both R0 and the endemic prevalence. Next, we present expressions for the breeding value and heritable variation, for endemic prevalence and individual binary disease status, and show that these depend strongly on the prevalence. Results show that heritable variation for endemic prevalence is substantially greater than currently believed, and increases strongly when prevalence decreases, while heritability of disease status approaches zero. As a consequence, response of the endemic prevalence to selection for lower disease status accelerates considerably when prevalence decreases, in contrast to classical predictions. Finally, we show that most heritable variation for the endemic prevalence is hidden in indirect genetic effects, suggesting a key role for kin-group selection in the evolutionary history of current populations and for genetic improvement in animals and plants.

scholarly journals Variation in Host Resistance to Blastomyces dermatitidis: Potential Use of Genetic Reference Panels and Advances in Immunophenotyping of Diverse Mouse Strains

mBio ◽  
2022 ◽  
Author(s):  
Elaine M. Kohn ◽  
Cleison Taira ◽  
Hanah Dobson ◽  
Lucas Dos Santos Dias ◽  
Uju Okaa ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Infectious Diseases ◽  
Fungal Infection ◽  
Host Resistance ◽  
Blastomyces Dermatitidis ◽  
Mouse Strains ◽  
Dimorphic Fungi ◽  
Host Genetic ◽  
Potential Use

Host genetic variation significantly impacts vulnerability to infectious diseases. While host variation in susceptibility to fungal infection with dimorphic fungi has long been recognized, genes that underpin this variation are poorly understood.

scholarly journals Host genetic regulation of immune-based and infectious diseases

2018 ◽  
Vol 29 (7-8) ◽  
pp. 365-366 ◽  
Author(s):  
Martin T. Ferris ◽  
Derek W. Hood
Keyword(s):  
Infectious Diseases ◽  
Genetic Regulation ◽  
Host Genetic

scholarly journals Bias, Accuracy, and Impact of Indirect Genetic Effects in Infectious Diseases

2012 ◽  
Vol 3 ◽  
Author(s):  
Debby Lipschutz-Powell ◽  
J. A. Woolliams ◽  
P. Bijma ◽  
R. Pong-Wong ◽  
M. L. Bermingham ◽  
...  
Keyword(s):  
Infectious Diseases ◽  
Genetic Effects ◽  
Indirect Genetic Effects

scholarly journals Statistical model and testing designs to increase response to selection with constrained inbreeding in genomic breeding programs for pigs affected by social genetic effects

2021 ◽  
Vol 53 (1) ◽  
Author(s):  
Thinh Tuan Chu ◽  
Mark Henryon ◽  
Just Jensen ◽  
Birgitte Ask ◽  
Ole Fredslund Christensen
Keyword(s):  
Statistical Model ◽  
Statistical Models ◽  
Genetic Effects ◽  
Response To Selection ◽  
Heritable Variation ◽  
Fixed Rate ◽  
Random Group ◽  
Breeding Programs ◽  
The Difference ◽  
Family Groups

Abstract Background Social genetic effects (SGE) are the effects of the genotype of one animal on the phenotypes of other animals within a social group. Because SGE contribute to variation in economically important traits for pigs, the inclusion of SGE in statistical models could increase responses to selection (RS) in breeding programs. In such models, increasing the relatedness of members within groups further increases RS when using pedigree-based relationships; however, this has not been demonstrated with genomic-based relationships or with a constraint on inbreeding. In this study, we compared the use of statistical models with and without SGE and compared groups composed at random versus groups composed of families in genomic selection breeding programs with a constraint on the rate of inbreeding. Results When SGE were of a moderate magnitude, inclusion of SGE in the statistical model substantially increased RS when SGE were considered for selection. However, when SGE were included in the model but not considered for selection, the increase in RS and in accuracy of predicted direct genetic effects (DGE) depended on the correlation between SGE and DGE. When SGE were of a low magnitude, inclusion of SGE in the model did not increase RS, probably because of the poor separation of effects and convergence issues of the algorithms. Compared to a random group composition design, groups composed of families led to higher RS. The difference in RS between the two group compositions was slightly reduced when using genomic-based compared to pedigree-based relationships. Conclusions The use of a statistical model that includes SGE can substantially improve response to selection at a fixed rate of inbreeding, because it allows the heritable variation from SGE to be accounted for and capitalized on. Compared to having random groups, family groups result in greater response to selection in the presence of SGE but the advantage of using family groups decreases when genomic-based relationships are used.

scholarly journals An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

animal ◽  
2009 ◽  
Vol 3 (3) ◽  
pp. 415-436 ◽  
Author(s):  
G. Davies ◽  
S. Genini ◽  
S.C. Bishop ◽  
E. Giuffra
Keyword(s):  
Genetic Variation ◽  
Infectious Diseases ◽  
Host Genetic

scholarly journals Host genetic effects in pneumonia

2021 ◽  
Vol 108 (1) ◽  
pp. 194-201
Author(s):  
Hung-Hsin Chen ◽  
Douglas M. Shaw ◽  
Lauren E. Petty ◽  
Misa Graff ◽  
Ryan J. Bohlender ◽  
...  
Keyword(s):  
Genetic Effects ◽  
Host Genetic

Genetic susceptibility to malaria and other infectious diseases: from the MHC to the whole genome

Parasitology ◽  
1996 ◽  
Vol 112 (S1) ◽  
pp. S75-S84 ◽  
Author(s):  
A. V. S. Hill
Keyword(s):  
Infectious Diseases ◽  
Twin Studies ◽  
Susceptibility Genes ◽  
Human Populations ◽  
Whole Genome ◽  
Case Control Studies ◽  
Powerful Approach ◽  
Affected Sibling Pair ◽  
Important Host ◽  
Host Genetic

There is substantial evidence that host genetic factors play a major role in determining the outcome of infection with many pathogens. Detailed analysis of malaria has identified twelve genes that affect susceptibility in various human populations. However, less attention has been paid to other major infectious diseases where twin studies have identified an important host genetic component to susceptibility. Recent progress in the analysis of the human genome offers exciting prospects for the mapping and identification of new susceptibility and resistance genes for common infectious diseases. Screening of the whole genome in affected sibling pair studies is now feasible by employing highly informative microsatellite markers. In addition, many polymorphic candidate genes have become available for analysis in case-control studies. It is proposed that these new genetic tools offer a powerful approach to the epidemiological analysis of many infectious diseases in humans and supersede traditional genetic approaches to identifying susceptibility genes in mouse models. Progress in characterizing the role of major histocompatibility genes in susceptibility to malaria and other infectious diseases is reviewed before outlining the methodologies for and progress in identifying non-MHC susceptibility genes.

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