BmADARa cooperatively inhibits BmNPV proliferation through the interaction of its dsRBD2 with BmDcr‐2‐DEXHc in silkworm, Bombyx mori

Adenosine deaminases that act on RNA (ADARs) are RNA editing enzymes capable of converting adenosine into inosine at specific sites within double-stranded RNA (dsRNA), widely distributed across various animal species. Dicer (Dcr), a member of the RNase III family and a crucial component of the RNA-induced silencing complex (RISC), allows ADAR to participate in innate immunity through Dcr-2 in Drosophila. Bombyx mori nucleopolyhedrovirus (BmNPV) is one of the viruses that can cause substantial economic losses to the sericulture industry upon infecting silkworm. Knocking down the expression of BmDcr-2 in silkworm enhances the proliferation of BmNPV. Our previous research revealed the existence of a predominantly expressed subtype, ADARa, in silkworm (BmADARa), which shares homology with Drosophila ADAR. It remains unclear whether BmADARa can also participate in innate immunity through BmDcr-2. Initially, through bacterial challenge experiments, we found that BmADARa exhibited the highest responsiveness to BmNPV stimulation. Further studies demonstrated that BmADARa, in conjunction with BmDcr-2-DEXHc (DEAD-box helicase domain), collectively inhibits the proliferation of BmNPV. BmADARa interacts with the DEXHc domain of BmDcr-2 through its dsRNA binding domain 2 (dsRBD2), thereby enhancing its ability to inhibit BmNPV proliferation. These results lay a foundation for the study of the function and molecular mechanism of BmADARa in innate immunity, and provide a new experimental ideas for antiviral research in B. mori.