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1.
Sci Adv ; 9(36): eadh8990, 2023 09 08.
Article in English | MEDLINE | ID: mdl-37683000

ABSTRACT

Disease emergence is accelerating with global changes. Understanding by which mechanisms host populations can rapidly adapt will be crucial for management practices. Pacific oyster mortality syndrome (POMS) imposes a substantial and recurrent selective pressure on oyster populations, and rapid adaptation may arise through genetics and epigenetics. In this study, we used (epi)genome-wide association mapping to show that oysters differentially exposed to POMS displayed genetic and epigenetic signatures of selection. Consistent with higher resistance to POMS, the genes targeted included many genes in several pathways related to immunity. By combining correlation, DNA methylation quantitative trait loci, and variance partitioning, we revealed that a third of phenotypic variation was explained by interactions between the genetic and epigenetic information, ~14% by the genome, and up to 25% by the epigenome alone. Similar to genetically based adaptation, epigenetic mechanisms notably governing immune responses can contribute substantially to the rapid adaptation of hosts to emerging infectious diseases.


Subject(s)
Genome-Wide Association Study , Ostreidae , Animals , Acclimatization , Epigenesis, Genetic , Syndrome , Genetic Variation
2.
Nat Commun ; 9(1): 4215, 2018 10 11.
Article in English | MEDLINE | ID: mdl-30310074

ABSTRACT

Infectious diseases are mostly explored using reductionist approaches despite repeated evidence showing them to be strongly influenced by numerous interacting host and environmental factors. Many diseases with a complex aetiology therefore remain misunderstood. By developing a holistic approach to tackle the complexity of interactions, we decipher the complex intra-host interactions underlying Pacific oyster mortality syndrome affecting juveniles of Crassostrea gigas, the main oyster species exploited worldwide. Using experimental infections reproducing the natural route of infection and combining thorough molecular analyses of oyster families with contrasted susceptibilities, we demonstrate that the disease is caused by multiple infection with an initial and necessary step of infection of oyster haemocytes by the Ostreid herpesvirus OsHV-1 µVar. Viral replication leads to the host entering an immune-compromised state, evolving towards subsequent bacteraemia by opportunistic bacteria. We propose the application of our integrative approach to decipher other multifactorial diseases that affect non-model species worldwide.


Subject(s)
Bacteremia/immunology , Crassostrea/immunology , Crassostrea/virology , Herpesviridae/physiology , Immunosuppression Therapy , Virus Diseases/immunology , Virus Diseases/virology , Animals , Antimicrobial Cationic Peptides/pharmacology , Crassostrea/microbiology , Hemocytes/drug effects , Hemocytes/pathology , Hemocytes/virology , Inhibitor of Apoptosis Proteins/metabolism , Phenotype , Virus Replication/drug effects
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