Fig. 8

Conceptual model of possible molecular events describing OsHV-1 and Crassostrea gigas interactions in the infected oyster cells. Replicating OsHV-1 DNA amplifies the production of viral RNAs, dsRNAs and proteins necessary for virion assembly and responsible of some host-pathogen interactions (e.g. OsHV-1 IAPs). The binding of viral DNAs and dsRNAs to specific oyster receptors, namely endogenous TLRs (eTLRs) and RIG-I/MDA5 proteins, activates the Toll and Interferon pathway, respectively (red boxes) and leads to the transcription of antiviral effectors (green boxes). Pro-apoptotic genes, like caspases, Pro-PO elements, like tyrosinases and laccases, and interferon stimulated genes, like viperin and ADAR-1 are upregulated during OsHV-1 infection. These antiviral effectors control the virus, which counteracts by expressing anti-apoptotic viral genes (IAPs, like ORF99). Oyster ADAR-1 edits dsRNAs with a mechanism known as A-to-I editing, producing G mismatches that impair dsRNAs, and possibly making the edited dsRNAs less effective in activating dsRNA receptors, while the impact on OsHV-1 replication is unknown. A few oyster miRNAs are regulated during OsHV-1 infection, but their function in controlling host and viral genes remain unclear