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 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 Modeling Host Genetic Regulation of Influenza Pathogenesis in the Collaborative Cross

2013 ◽  
Vol 9 (2) ◽  
pp. e1003196 ◽  
Author(s):  
Martin T. Ferris ◽  
David L. Aylor ◽  
Daniel Bottomly ◽  
Alan C. Whitmore ◽  
Lauri D. Aicher ◽  
...  
Keyword(s):  
Genetic Regulation ◽  
Collaborative Cross ◽  
Host Genetic

scholarly journals Genetic analysis of IgG subclass responses against RESA and MSP2 of Plasmodium falciparum in adults in Papua New Guinea

2000 ◽  
Vol 124 (1) ◽  
pp. 153-162 ◽  
Author(s):  
H. A. STIRNADEL ◽  
H.-P. BECK ◽  
M. P. ALPERS ◽  
T. A. SMITH
Keyword(s):  
Plasmodium Falciparum ◽  
Papua New Guinea ◽  
Vaccine Development ◽  
Familial Aggregation ◽  
Major Gene ◽  
Genetic Regulation ◽  
New Guinea ◽  
Variance Component Analysis ◽  
Igg Subclass ◽  
Host Genetic

Contributions of environmental and genetic factors to IgG subclass responses against Plasmodium falciparum antigens RESA and MSP2 were investigated among adults in a highly endemic area of Papua New Guinea. Heritabilities were estimated using variance component analysis. Familial aggregation of several responses was found, including IgG1, IgG2 and IgG3 responses against RESA, IgG1 and IgG3 responses against the 3D7 form of MSP2 and IgG1, IgG2 responses against the FC27 form of MSP2. Allowance for sharing of houses explained some of the non-genetic variance but not the familial aggregation. The variance of IgG3 responses against RESA and IgG1, IgG2 against MSP2 (FC27) was partly explained by sharing of HLA class II genotypes, although heritability was low. Segregation analyses indicated that any genetic regulation was more complex than governed by a single major gene. Such host genetic variation in responses to specific malaria antigens has implications for immuno-epidemiology and vaccine development.

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

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.

scholarly journals Genetics of Sub-Saharan African Human Population: Implications for HIV/AIDS, Tuberculosis, and Malaria

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Gerald Mboowa
Keyword(s):  
Infectious Disease ◽  
Genetic Diversity ◽  
Infectious Diseases ◽  
Sub Saharan Africa ◽  
Susceptible Host ◽  
Host Genetics ◽  
Evolutionary Forces ◽  
Host Genetic ◽  
Sub Saharan ◽  
Hiv Aids

Sub-Saharan Africa has continued leading in prevalence and incidence of major infectious disease killers such as HIV/AIDS, tuberculosis, and malaria. Epidemiological triad of infectious diseases includes susceptible host, pathogen, and environment. It is imperative that all aspects of vertices of the infectious disease triad are analysed to better understand why this is so. Studies done to address this intriguing reality though have mainly addressed pathogen and environmental components of the triad. Africa is the most genetically diverse region of the world as well as being the origin of modern humans. Malaria is relatively an ancient infection in this region as compared to TB and HIV/AIDS; from the evolutionary perspective, we would draw lessons that this ancestrally unique population now under three important infectious diseases both ancient and exotic will be skewed into increased genetic diversity; moreover, other evolutionary forces are also still at play. Host genetic diversity resulting from many years of malaria infection has been well documented in this population; we are yet to account for genetic diversity from the trio of these infections. Effect of host genetics on treatment outcome has been documented. Host genetics of sub-Saharan African population and its implication to infectious diseases are an important aspect that this review seeks to address.

scholarly journals The genetic architecture of human infectious diseases and pathogen-induced cellular phenotypes

2020 ◽  
Author(s):  
Andrew T Hale ◽  
Dan Zhou ◽  
Rebecca L Sale ◽  
Lisa Bastarache ◽  
Liuyang Wang ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Infectious Diseases ◽  
Molecular Mechanisms ◽  
Causal Effect ◽  
Association Studies ◽  
Rrna Gene ◽  
Pathogen Invasion ◽  
Gene Level ◽  
Host Genetic ◽  
Cellular Phenotypes

Infectious diseases (ID) represent a significant proportion of morbidity and mortality across the world. Host genetic variation is likely to contribute to ID risk and downstream clinical outcomes, but there is a need for a genetics-anchored framework to decipher molecular mechanisms of disease risk, infer causal effect on potential complications, and identify instruments for drug target discovery. Here we perform transcriptome-wide association studies (TWAS) of 35 clinical ID traits in a cohort of 23,294 individuals, identifying 70 gene-level associations with 26 ID traits. Replication in two large-scale biobanks provides additional support for the identified associations. A phenome-scale scan of the 70 gene-level associations across hematologic, respiratory, cardiovascular, and neurologic traits proposes a molecular basis for known complications of the ID traits. Using Mendelian Randomization, we then provide causal support for the effect of the ID traits on adverse outcomes. The rich resource of genetic information linked to serologic tests and pathogen cultures from bronchoalveolar lavage, sputum, sinus/nasopharyngeal, tracheal, and blood samples (up to 7,699 positive pathogen cultures across 92 unique genera) and a large catalog of genome-wide associations of microbiome variation generated from phylogenetic analysis of 16S rRNA gene sequences are developed here into a platform to interrogate the genetic basis of compartment-specific infection and colonization. To accelerate insights into cellular mechanisms, we develop a TWAS repository of gene-level associations in a broad collection of human tissues with 79 pathogen-exposure induced cellular phenotypes as a discovery and replication platform. Cellular phenotypes of infection by 8 pathogens included pathogen invasion, intercellular spread, cytokine production, and pyroptosis. These rich datasets will facilitate mechanistic insights into the role of host genetic variation on ID risk and pathophysiology, with important implications for our molecular understanding of potentially severe phenotypic outcomes.

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