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

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.