bioRxivGenomicsPreprint
Multi-Omics Reprogramming Drives a Counterintuitive Reversal of Disease Susceptibility During Ageing
A. ValdiviesoiD, Léo DuperretiD, Bruno PettoniD, Gaëlle Courtay, Océane RomatifiD, Juliette PouzadouxiD, Sylvain Henry, Andrei TurtoïiD, Ève ToulzaiD, Arnaud LagorceiD, Lionel DégremontiD, Benjamín MorgaiD, Emmanuel VignaliD, Céline CosseauiD, Fabrice PernetiD, Guillaume MittaiD, Jérémie Vidal‐DupioliD
Abstract
Ageing is a progressive and irreversible biological process characterized by the deterioration of physiological functions and increased vulnerability to mortality. Although extensively studied in vertebrates, ageing in long-lived invertebrates remains comparatively unexplored. While ageing typically leads to greater susceptibility to infectious diseases, a striking and unexpected reversal was identified in oysters: older oysters exhibit markedly increased tolerance to the Pacific Oyster Mortality Syndrome (POMS), a panzootic disease primarily driven by the OsHV-1 herpesvirus and responsible for severe losses in global aquaculture. To investigate this counterintuitive pattern, we challenged oysters aged 4, 16, and 28 months from four biparental families and conducted an integrative multi-omics analysis, including epigenomics, transcriptomics, and metabolomics on the two families showing the strongest age-related increase in survival. Our results reveal that ageing in Magallana gigas is characterized by coordinated epigenetic, transcriptional, and metabolic reprogramming that reduces host permissiveness to POMS. We show that the epigenetic remodeling of key immune regulators (e.g., Toll-like receptors, MyD88) aligns with transcriptional rewiring of NF-{kappa}B and ubiquitin pathways, producing a finely tuned innate immune state marked by enhanced antiviral activity but reduced antibacterial responsiveness. We also identify age-related repression of mTOR signaling, likely promoting autophagy and improving viral control. These regulatory changes are tightly linked to metabolic adjustments, including reduced TCA cycle flux, remodeled nitrogen metabolism, and altered glutathione dynamics, which collectively support a stress-tolerant, energy-conserving phenotype. Together, our findings reveal a fundamental evolutionary trade-off: juveniles prioritize growth at the cost of viral susceptibility, whereas adults invest in cellular maintenance and antiviral preparedness.
- organism: bacteria (other)
- assay: metabolomics
- assay: proteomics
- assay: DNA methylation
- assay: bulk RNA-seq
- research focus: gene regulatory network inference
- research focus: differential expression
- research focus: cell-cell communication
- approach: statistical model
- Citations
- 0
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Aging associated altered response to intracellular bacterial infections and its implication on the host
S. E. Fernandes, A. Singh, … D. K. Saini·bioRxiv·Sep 15, 2020
- Enteric viral infections promote systemic accelerated aging in Drosophila
Rubén González, Mauro Castelló-Sanjuán, Maria‐Carla Saleh·Science AdvancesPeer-reviewed·Jun 5, 2026
- Harnessing variation in Drosophila melanogaster reveals different routes to increased infection susceptibility over age and sex-dependent association with lifespan
Barbara Monteiro-Black, Mary-Kate Corbally, … Jennifer C. Regan·bioRxiv·Jul 7, 2025
- Aging-associated dysbiosis increases susceptibility to enteric viral infection in Drosophila
Christine Sansone, Jonathan Cohen, … Sara Cherry·bioRxiv·Jun 27, 2017
- EARLY INFLAMMATION, IMMUNOPATHOLOGY AND AGING
Imroze Khan, Deepa Agashe, Jens Rolff·bioRxiv·Sep 22, 2016
- The evolution of age-specific resistance to infectious disease
L. J. Buckingham, E. L. Bruns, B. Ashby·bioRxiv·Oct 5, 2022