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Fish Shellfish Immunol. 2014 Jan;36(1):151-7. doi: 10.1016/j.fsi.2013.10.026. Epub 2013 Nov 5.

Ontogeny and water temperature influences the antiviral response of the Pacific oyster, Crassostrea gigas.

Author information

1
School of Biological Sciences and Australian Seafood Cooperative Research Centre, Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia. Electronic address: tim.green@flinders.edu.au.
2
Ifremer, UMR 5119 Ecology of Coastal Marine Systems, Université Montpellier 2, Place Eugène Bataillon, CC80, 30495 Montpellier cedex 05, France.
3
Marine Ecology Research Centre, Southern Cross University, P.O. Box 157, Lismore, NSW 2480, Australia.
4
School of Biological Sciences and Australian Seafood Cooperative Research Centre, Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia; Nofima, P.O. Box 210, N-1431 Ås, Norway.
5
School of Biological Sciences and Australian Seafood Cooperative Research Centre, Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia.

Abstract

Disease is caused by a complex interaction between the pathogen, environment, and the physiological status of the host. Determining how host ontogeny interacts with water temperature to influence the antiviral response of the Pacific oysters, Crassostrea gigas, is a major goal in understanding why juvenile Pacific oysters are dying during summer as a result of the global emergence of a new genotype of the Ostreid herpesvirus, termed OsHV-1 μvar. We measured the effect of temperature (12 vs 22 °C) on the antiviral response of adult and juvenile C. gigas injected with poly I:C. Poly I:C up-regulated the expression of numerous immune genes, including TLR, MyD88, IκB-1, Rel, IRF, MDA5, STING, SOC, PKR, Viperin and Mpeg1. At 22 °C, these immune genes showed significant up-regulation in juvenile and adult oysters, but the majority of these genes were up-regulated 12 h post-injection for juveniles compared to 26 h for adults. At 12 °C, the response of these genes was completely inhibited in juveniles and delayed in adults. Temperature and age had no effect on hemolymph antiviral activity against herpes simplex virus (HSV-1). These results suggest that oysters rely on a cellular response to minimise viral replication, involving recognition of virus-associated molecular patterns to induce host cells into an antiviral state, as opposed to producing broad-spectrum antiviral compounds. This cellular response, measured by antiviral gene expression of circulating hemocytes, was influenced by temperature and oyster age. We speculate whether the vigorous antiviral response of juveniles at 22 °C results in an immune-mediated disorder causing mortality.

KEYWORDS:

Antiviral response; Crassostrea; Herpesvirus; OsHV-1; Water temperature

PMID:
24200990
DOI:
10.1016/j.fsi.2013.10.026
[Indexed for MEDLINE]

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