Abstract
Since 2008, massive mortality outbreaks associated with OsHV-1 detection have been reported in Crassostrea gigas spat and juveniles in several countries. Nevertheless, adult oysters do not demonstrate mortality in the field related to OsHV-1 detection and were thus assumed to be more resistant to viral infection. Determining how virus and adult oyster interact is a major goal in understanding why mortality events are not reported among adult Pacific oysters. Dual transcriptomics of virus-host interactions were explored by real-time PCR in adult oysters after a virus injection. Thirty-nine viral genes and five host genes including MyD88, IFI44, IkB2, IAP and Gly were measured at 0.5, 10, 26, 72 and 144 hours post infection (hpi). No viral RNA among the 39 genes was detected at 144 hpi suggesting the adult oysters are able to inhibit viral replication. Moreover, the IAP gene (oyster gene) shows significant up-regulation in infected adults compared to control adults. This result suggests that over-expression of IAP could be a reaction to OsHV-1 infection, which may induce the apoptotic process. Apoptosis could be a main mechanism involved in disease resistance in adults. Antiviral activity of haemolymph against herpes simplex virus (HSV-1) was not significantly different between infected adults versus control.
Highlights
In 1972, virus particles morphologically similar to herpesviruses were first reported in an invertebrate, the Eastern oyster, Crassostrea virginica, from the USA [1]
No mortality was observed in control adult oysters, viral DNA was detected by real-time PCR in animals from both families (A1 and A2) (Figure 2)
As Pacific oysters do not show macroscopic symptoms before dying during the course of ostreid herpesvirus type 1 (OsHV-1) infection, it remains difficult in the absence of mortality reports to know whether adults are susceptible to infection
Summary
In 1972, virus particles morphologically similar to herpesviruses were first reported in an invertebrate, the Eastern oyster, Crassostrea virginica, from the USA [1]. OsHV-1 is reported in mass mortality outbreaks observed among Pacific oysters less than one year old [5,6,7,8]. Considering the economic importance of shellfish culture, tools have been previously developed for rapid virus detection [5,9,10,11,12] and the OsHV-1 genome has been fully sequenced from purified virus particles [3]. Since 2008, mass mortality outbreaks (with rates of up to 80%) were reported in C. gigas spat and juveniles in Europe, New Zealand and Australia [13,14,15] and were associated with virus variants [16,17,18]. The role of OsHV-1 in these mortalities has been underlined by experimental
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