Figure 5.

Interplay between shrimp NF-κB pathways and WSSV. The activation of the NF-κB pathway can be hijacked by WSSV to favor its gene expression and genome replication. WSSV infection activates the host Toll pathway, which leads to the activation of Dorsal that translocates into the nucleus to induce viral-gene expression and promote viral-genome replication. A similar situation is observed for the IMD pathway. The activation of wsv069 mediated by the NF-κB pathways can in turn induce its own expression, which creates a self-regulatory loop. Such a positive-feedback loop amplifies the signaling extent to further activate other viral genes. Until now, after WSSV infection, the NF-κB pathways have been shown to be subject to numerous regulatory controls by both host factors—such as p53, miR1959, and HMGB—and viral factor, such as WSSV449, WSSV-miR-N13, and WSSV-miR-N23. However, the activation of the shrimp canonical NF-κB pathway can also lead to AMP expression, such as ALFs, which have strong antiviral activity against WSSV. Therefore, WSSV could have evolved some currently unknown strategies to attenuate the antiviral role of the host NF-κB pathway to instead engage its activation to favor viral pathogenesis.