Temperature modulate disease susceptibility of the Pacific oyster Crassostrea gigas and virulence of the Ostreid herpesvirus type 1

• Published in: Fish & Shellfish Immunology
• Main Authors: Delisle, Lizenn, Petton, Bruno, Burguin, Jean Francois, Morga, Benjamin, Corporeau, Charlotte, Pernet, Fabrice
• Format: Text
• Language: English
• Published: Academic Press Ltd- Elsevier Science Ltd
• Subjects: envir; psy; Pacific; Crassostrea gigas; Pacific oyster
• Online Access: https://doi.org/10.1016/j.fsi.2018.05.056; https://archimer.ifremer.fr/doc/00442/55337/56847.pdf; https://archimer.ifremer.fr/doc/00442/55337/

Temperature triggers marine diseases by changing host susceptibility and pathogen virulence. Oyster mortalities associated with the Ostreid herpesvirus type 1 (OsHV-1) have occurred seasonally in Europe when the seawater temperature range reaches 16–24 °C. Here we assess how temperature modulates oyster susceptibility to OsHV-1 and pathogen virulence. Oysters were injected with OsHV-1 suspension incubated at 21 °C, 26 °C and 29 °C and were placed in cohabitation with healthy oysters (recipients) at these three temperatures according to a fractional factorial design. Survival was followed for 14 d and recipients were sampled for OsHV-1 DNA quantification and viral gene expression. The oysters were all subsequently placed at 21 °C to evaluate the potential for virus reactivation, before being transferred to oyster farms to evaluate their long-term susceptibility to the disease. Survival of recipients at 29 °C (86%) was higher than at 21 °C (52%) and 26 °C (43%). High temperature (29 °C) decreased the susceptibility of oysters to OsHV-1 without altering virus infectivity and virulence. At 26 °C, the virulence of OsHV-1 was enhanced. Differences in survival persisted when the recipients were all placed at 21 °C, suggesting that OsHV-1 did not reactivate. Additional oyster mortality followed the field transfer, but the overall survival of oysters infected at 29 °C remained higher.