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Seminar Abstract: Cells have evolved two key cell-intrinsic antiviral pathways triggered by double-stranded RNA (dsRNA): the interferon (IFN) system and RNA interference (RNAi). These pathways are mutually antagonistic and operate in different cellular contexts. We explored whether they limit the efficacy of self-amplifying RNA (sa-RNA), a promising next-generation vaccine platform. We show that sa-RNAs are restricted by RNAi in stem cells and by the IFN-induced kinase PKR in somatic cells. Cis-expression of the Nodamura virus B2 protein overcomes both barriers by sequestering replication-derived dsRNA at the cell periphery, preventing translational shutdown without impairing IFN signalling or the self-adjuvant properties of sa-RNA. These findings suggest a potential strategy to improve sa-RNA efficacy while preserving its immunostimulatory potential.

Biosketch: Dr Pierre Maillard is a UKRI Future Leaders Fellow and Senior Lecturer at the Blizard Institute, Queen Mary University of London (QMUL), where his group studies how cells combat viral infections with the long-term vision of developing innovative antiviral therapeutic strategies. He completed his PhD at the ?cole Polytechnique Fédérale de Lausanne (EPFL), Switzerland, investigating cell-intrinsic defence mechanisms against retroviruses, before pursuing postdoctoral research at ETH Zürich, where he studied the antiviral role of RNA interference in mammals and subsequently at the Francis Crick Institute in London, exploring the interplay between antiviral RNA interference and the interferon system. In 2017, he was awarded a Wolfson UCL Excellence Fellowship to begin his independent research programme in the Division of Infection and Immunity at University College London and before establishing his group at QMUL’s Blizard Institute.