As shown against several RNA viruses, the RNA interference (RNAi) pathway plays a crucial role in antiviral responses in insects. Cleavage of double-stranded RNA genomes or intermediates produced during replication into viral short interfering RNAs is part of the response (v-siRNAs). We discovered that a large number of small reads of less than 20 nucleotides from Helicoverpa armigeralarvae infected with Helicoverpa armigera single nucleopolyhedrovirus (HaSNPV) were mapped to specific open reading frames in the viral genome (hot spots) that are mostly structural and auxiliary late genes using deep sequencing.

Dicer-2, the key enzyme implicated in the RNAi response in insects, was found to be involved in the creation of v-siRNAs after the potential of these short RNAs being microRNAs was ruled out. Higher transcript levels of the hot spot genes were discovered in Dicer-2-silenced cells, but not in Dicer-1-silenced cells, and the virus replicated more efficiently as a result. The findings imply that the RNAi response of the host degrades viral transcripts. However, this could work in the virus’s favour by limiting overreplication, which would otherwise cause the host cells to die prematurely.