FN Archimer Export Format
PT J
TI Temperature modulate disease susceptibility of the Pacific oyster Crassostrea gigas and virulence of the Ostreid herpesvirus type 1
BT 
AF DELISLE, Lizenn
   PETTON, Bruno
   BURGUIN, Jean Francois
   MORGA, Benjamin
   CORPOREAU, Charlotte
   PERNET, Fabrice
AS 1:1;2:2;3:1;4:3;5:1;6:1;
FF 1:PDG-RBE-PFOM-LPI;2:PDG-RBE-PFOM-LPI;3:PDG-RBE-PFOM-PI;4:PDG-RBE-SGMM-LGPMM;5:PDG-RBE-PFOM-LPI;6:PDG-RBE-PFOM-LPI;
C1 IFREMER, LEMAR, UMR 6539, Technopole Brest Iroise, F-29280 Plouzane, France.
   IFREMER, LEMAR, UMR 6539, F-29840 Presquile Du Vivier, Argenton, France.
   IFREMER, LGPMM, Ave Mus Loup, F-17390 La Tremblade, France.
C2 IFREMER, FRANCE
   IFREMER, FRANCE
   IFREMER, FRANCE
SI BREST
   ARGENTON
   LA TREMBLADE
SE PDG-RBE-PFOM-LPI
   PDG-RBE-PFOM-PI
   PDG-RBE-SGMM-LGPMM
UM LEMAR
IN WOS Ifremer jusqu'en 2018
IF 3.298
TC 28
UR https://archimer.ifremer.fr/doc/00442/55337/56847.pdf
LA English
DT Article
DE ;Bivalve;Health;Marine disease;Mortality risk;Temperature;Virulence
AB 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. 
PY 2018
PD SEP
SO Fish & Shellfish Immunology
SN 1050-4648
PU Academic Press Ltd- Elsevier Science Ltd
VL 80
UT 000440958100009
BP 71
EP 79
DI 10.1016/j.fsi.2018.05.056
ID 55337
ER

EF