Our goal is to understand the molecular mechanisms whereby the genomic RNA of influenza-like viruses is, on the one hand, the template for transcription and replication of the viral genome by its RNA-dependent RNA polymerase and, on the other hand, an Achilles’ heel, whose recognition as non-self can trigger an innate immune response to counter the viral infection. Molecular warfare between the virus and the host-cell occurs at many levels. Influenza polymerase has a unique mechanism of transcription priming called ‘cap-snatching’, which involves pirating short-capped oligomers from nascent cellular Pol II transcripts; this contributes to shutdown of host-cell gene expression. The cell counters RNA viruses with innate immune pattern-recognition receptors, such as the RNA helicase RIG-I, which recognise particular viral RNA structural motifs (e.g. 5′ triphosphate-dsRNA) as non-self, thus activating a signalling pathway leading to interferon production and establishment of the anti-viral state. In response, viruses deploy proteins as counter-counter-measures to dampen the immune response, for instance, by supressing the RIG-I signalling pathway.