文摘
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 渭var. We measured the effect of temperature (12 vs 22聽掳C) on the antiviral response of adult and juvenile C.聽gigas injected with poly I:C. Poly I:C up-regulated the expression of numerous immune genes, including TLR, MyD88, I魏B-1, Rel, IRF, MDA5, STING, SOC, PKR, Viperin and Mpeg1. At 22聽掳C, these immune genes showed significant up-regulation in juvenile and adult oysters, but the majority of these genes were up-regulated 12聽h post-injection for juveniles compared to 26聽h for adults. At 12聽掳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聽掳C results in an immune-mediated disorder causing mortality.