Fig. 4.

Model for viral infection effects on TEs in carcasses. (A) In uninfected conditions, TEs are controlled by piRNAs and siRNAs. (B) Upon infection, the dsRNA uptake pathway allows the systemic spread of viral RNAs, and this machinery also opportunistically carries TE dsRNA intermediates and allows for their spread. This triggers the systemic production of virus-derived siRNAs as well as TE-derived siRNAs, which subsequently leads to the reduction of TE transcript amounts in carcasses. The uptaken TE RNAs are also substrates for piRNA synthesis, which strengthen TE posttranscriptional silencing. (C) In case the siRNA pathway is impaired (e.g., dcr2^−/− mutant, or viral RNAi suppressor targeting Dcr-2), viral replication increases, and we propose that viral RNAs saturate the piRNA pathway, which is no longer available for TEs. This results in an increase in TE transcript amounts.