High temperature induces transcriptomic changes in Crassostrea gigas that hinder progress of ostreid herpesvirus (OsHV-1) and promote survival

Of all environmental factors, seawater temperature plays a decisive role in triggering marine diseases. Like fever in vertebrates, high seawater temperature could modulate the host response to pathogens in ectothermic animals. In France, massive mortality of Pacific oysters, Crassostrea gigas, cause...

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Bibliographic Details
Published in:Journal of Experimental Biology
Main Authors: Delisle, Lizenn, Pauletto, Marianna, Vidal-dupiol, Jeremie, Petton, Bruno, Bargelloni, Luca, Montagnani, Caroline, Pernet, Fabrice, Corporeau, Charlotte, Fleury, Elodie
Format: Article in Journal/Newspaper
Language:English
Published: The Company of Biologists 2020
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Online Access:https://archimer.ifremer.fr/doc/00656/76806/77974.pdf
https://doi.org/10.1242/jeb.226233
https://archimer.ifremer.fr/doc/00656/76806/
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Summary:Of all environmental factors, seawater temperature plays a decisive role in triggering marine diseases. Like fever in vertebrates, high seawater temperature could modulate the host response to pathogens in ectothermic animals. In France, massive mortality of Pacific oysters, Crassostrea gigas, caused by the ostreid herpesvirus 1 (OsHV-1) is markedly reduced when temperatures exceed 24°C in the field. In the present study we assess how high temperature influences the host response to the pathogen by comparing transcriptomes (RNA sequencing) during the course of experimental infection at 21°C (reference) and 29°C. We show that high temperature induced host physiological processes that are unfavorable to the viral infection. Temperature influenced the expression of transcripts related to the immune process and increased the transcription of genes related to the apoptotic process, synaptic signaling and protein processes at 29°C. Concomitantly, the expression of genes associated with catabolism, metabolite transport, macromolecule synthesis and cell growth remained low from the first stage of infection at 29°C. Moreover, viral entry into the host might have been limited at 29°C by changes in extracellular matrix composition and protein abundance. Overall, these results provide new insights into how environmental factors modulate host–pathogen interactions.