Abstract
Antiviral immunity involves various mechanisms and responses, including the RNA interference (RNAi) pathway. During long-term coevolution, viruses have gained the ability to evade this defense by encoding viral suppressors of RNAi (VSRs). It was reported that p35 of baculovirus can inhibit cellular small interference RNA (siRNA) pathway; however, the molecular mechanisms underlying p35 as a VSR remain largely unclear. Here, we showed that p35 of Bombyx mori nucleopolyhedrovirus (BmNPV) reduces the accumulation of virus-derived siRNAs (vsiRNAs) mapped to a particular region in the viral genome, leading to an increased expression of the essential genes in this region, and revealed that p35 disrupts the function of siRNAs by preventing them from loading into Argonaute-2 (Ago2). This repressive effect on the cellular siRNA pathway enhances the replication of BmNPV. Thus, our findings illustrate for the first time the inhibitory mechanism of a baculovirus VSR and how this effect influences viral infection.
Highlights
All living organisms are constantly exposed to all sorts of microbial pathogens
These results illustrated that Bombyx mori nucleopolyhedrovirus (BmNPV) is a target of RNA interference (RNAi) like the viruses mentioned above, and its infection progress can be restricted by the small interference RNA (siRNA) pathway of the host
The siRNA pathway seems to make no difference on viral invasion at a relatively late stage, and it may be due to the overwhelming viral load that is unaffordable for the RNAi-mediated antiviral immunity
Summary
The conflict between viral pathogens and their hosts leads to the coevolution of antiviral defenses and viral suppression mechanisms of host resistance. It has been validated that both RNA viruses such as Drosophila X virus (DXV) [1] and cricket paralysis virus (CrPV) [2] and DNA viruses such as invertebrate iridescent virus 6 (IIV6) [3] are targets of insect RNAi machinery. In antiviral RNAi response of insects, Dicer-2 (Dcr-2) and Argonaute-2 (Ago2) are two key proteins. Double-stranded RNAs (dsRNAs) produced in viral infection are detected and processed into approximately 20 nucleotides (nt) virus-derived siRNAs (vsiRNAs) by the nuclease Dcr-2 [4]. Following dsRNA cleavage, the generated siRNAs are loaded into Ago to form the RNA-induced silencing complex (RISC), which induces the antiviral defense machinery to cleave specific complementary viral RNAs with the RNase activity of Ago2 [5, 6]
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