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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Immunol Rev. 2009 Jan;227(1):176–188. doi: 10.1111/j.1600-065X.2008.00722.x

Fig. 5. Model for the induction and suppression of the Dicer-initiated viral immunity in Drosophila against Flock house virus.

Fig. 5

Asymmetric RNA synthesis in the replication of (+)RNA viruses involves multiple initiation of the progeny (+)RNA synthesis on the low abundant (-)RNA template complexed with the viral RdRP and other host factors. The resulting dsRNA of approximate 400 nt in length formed between the 5′-terminal nascent progeny (+)RNA1 and the (-)RNA1 template in FHV-infected cells, termed the initiating vRI-dsRNA, serves as substrates of DCR2. This results in the predominant production of 5′-terminal viRNAs, thereby triggering the RNAi-mediated viral immunity and abortive infection by FHV-ΔB2. In addition to binding to viRNAs, B2 is part of the viral RNA replication complex by direct interactions with viral RdRP (protein A) and vRI-dsRNA and inhibits DCR2-dependent production of viRNAs, thus ensuring successful infection by FHV. We propose that sequestering the initiating vRI-dsRNA and inhibiting their processing into the 5′-terminal viRNAs by B2 play a particularly important role in the suppression of the viral immunity. Reprinted from (32). RdRP, RNA-dependent RNA polymerase; FHV, Flock house virus; DCR, Dicer.