Pacific oyster mortality syndrome (POMS), caused by Ostreid herpesvirus-1 (OsHV-1), represents one of the most significant threats to global oyster aquaculture. Our research group has recently demonstrated that oysters are amenable to immune priming, supporting the potential for vaccination-based approaches. Autogenous vaccination therefore offers a promising strategy to confer protection, yet the host immune mechanisms underlying vaccine-induced protection remain poorly understood. Here, we evaluated the protective efficacy and host transcriptional basis of immune priming in Crassostrea gigas using heat-treated and live OsHV-1 vaccines across two temperature conditions, combining survival analysis with whole-transcriptome profiling.
All vaccinated groups showed significantly improved survival following OsHV-1 challenge compared to unvaccinated controls, with relative percent survival values of 76.2% and 85% for a heat-treated vaccine delivered at 22°C and a live OsHV-1 vaccine delivered at 18°C. Vaccinated oysters also showed markedly reduced viral loads and lower OsHV-1 viral transcript abundance following challenge compared to unvaccinated controls, with the live OsHV-1 priming group exhibiting significantly lower viral DNA concentrations in moribund oysters (p = 0.001), collectively indicating effective suppression of viral replication in primed animals. Transcriptome profiling across 51 samples revealed temporally dynamic and treatment-specific transcriptional responses. During priming, the live vaccine group mounted an earlier response (1,167 differentially expressed genes, DEGs, at 1 dpp vs. 537 in the heat-treated group), whereas the heat-treated group exhibited a substantially amplified peak response of 3,908 DEGs at 4 dpp. Following viral challenge, the unvaccinated positive control showed the largest transcriptional response, peaking at 879 DEGs at 4 dpc and remaining elevated at 316 DEGs by 12 dpc, while both vaccinated groups resolved to 45 and 82 DEGs by the same timepoint.
These quantitative differences revealed that the two vaccine formulations engaged distinct molecular entry points into the host immune response. Live OsHV1 rapidly activated RLR/MAVSlike antiviral pathways and interferonstimulatedlike transcriptional responses within 1 day postpriming, consistent with direct recognition of viral nucleic acid, whereas the heattreated group triggered a delayed but markedly amplified remodelling of proteostasis networks, ubiquitin–proteasome machinery and intracellular trafficking at 4 days postpriming. Upon subsequent viral challenge, the live vaccine group showed strong early upregulation of DNA replication and cell cycle modules, including genes most similar by orthology inference to replication licensing factors MCM2, MCM4 and MCM7, and DNA polymerase epsilon—consistent with expansion of the haemocyte compartment—alongside IFI44Lfamily and DHX58/LGP2like antiviral response genes. In contrast, unvaccinated oysters sustained a prolonged interferonstimulatedlike response characterised by upregulation of interferonstimulatedlike genes and dsRNA sensorfamily genes, alongside BIRC2like inhibitor of apoptosis genes, persisting through 12 days postchallenge without resolution. These findings demonstrate that autogenous OsHV-1 vaccination reconfigures rather than suppresses the host transcriptional response to viral challenge, providing a functional transcriptional basis for vaccine-induced resilience against POMS and supporting the development of autogenous vaccination as a viable biocontrol strategy for oyster aquaculture.
Acknowledgment
This work was funded by 2024 Proof of Concept Fund (DVCR POC 45-2024 Strategic Fund), The University of Sydney.