Infections with avian pathogenic (APEC) can be extremely detrimental to poultry health and production. Investigating host genetic variation could identify the biological mechanisms that control resistance to this pathogen and allow selection for improved resistance in experimental and commercial poultry populations. In this review, the current knowledge of how host genetics contributes to APEC resistance and future opportunities that would benefit the understanding or application of genetic resistance are discussed. Phenotypes, such as antibody responses, lesion scores, and mortality, revealed that genetic background impacts APEC resistance and interacts with other factors including the environment and challenge conditions. Experiments have used divergent selection for APEC-specific antibody levels to facilitate genetic studies, estimated heritabilities in relevant traits, detected quantitative trait loci using microsatellites, and made associations with sequence variation in the major histocompatibility complex, which collectively suggest that improving APEC resistance through selection is feasible, although genetic control is partial, complex, and highly polygenic. Additionally, functional genomics techniques have identified antimicrobial responses, toll-like receptor and cytokine signalling, and the cell cycle as central pathways in the host response to APEC challenge. Opportunities for future research are discussed, including the expansion of existing lines of research and the application of new technologies that are relevant to the study of host genetics and APEC. This review closes with prospective strategies for improvement of host genetic resistance to APEC.
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http://dx.doi.org/10.1080/03079457.2021.1879990 | DOI Listing |
Front Cell Infect Microbiol
December 2024
Servicio de Microbiología, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Madrid, Spain.
Introduction: Murepavadin is an antimicrobial peptide (AMP) in clinical development that selectively targets LptD and whose resistance profile remains unknown. We aimed to explore genomic modifications and consequences underlying murepavadin and/or colistin susceptibility.
Methods: To define genomic mechanisms underlying resistance, we performed two approaches: 1) a genome-wide association study (GWAS) in a clinical collection (n=496), considering >0.
Front Plant Sci
December 2024
National Key Laboratory of Crop Genetic Improvement, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, China.
Introduction: Drought stress severely hampers seedling growth and root architecture, resulting in yield penalties. Seed priming is a promising approach to tolerate drought stress for stand establishment and root development.
Methods: Here, various seed priming treatments, .
Curr Protoc
December 2024
Institute of Virology, Medical University of Innsbruck, Innsbruck, Austria.
Antiviral drugs are essential medications to save the lives of infected people. However, they are under constant threat to become ineffective as viruses evolve quickly. Studying the development of resistance is therefore paramount to understand the impact of mutations on pharmacological treatment and to make informed decisions.
View Article and Find Full Text PDFNucleic Acids Res
December 2024
Junior Research Group RNA Biology of Fungal Infections, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (Leibniz-HKI), Beutenbergstraße 11A, 07745 Jena, Germany.
Increasing antifungal drug resistance is a major concern associated with human fungal pathogens like Aspergillus fumigatus. Genetic mutation and epimutation mechanisms clearly drive resistance, yet the epitranscriptome remains relatively untested. Here, deletion of the A.
View Article and Find Full Text PDFFuture Oncol
December 2024
Department of Medical Oncology, BC Cancer Agency, Vancouver, Canada.
Metastatic prostate cancer remains incurable. Though significant progress has been made in the field, the search for agents that improve outcomes for patients is ongoing. Several clinical trials have explored the benefit of combining PARP inhibitors (PARPi) with androgen receptor pathway inhibitors (ARPIs) for metastatic castrate resistant prostate cancer (mCRPC), especially those cancers with alterations in homologous recombination repair (HRR) genes.
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