The Pathogen Recognition Receptor RIG-I is Functional in Platelets and Limits Thrombotic Responses.

Influenza-derived vRNA activates functional RIG-I in human platelets, driving MAVS-dependent pMLKL oligomerization and S100A10 release that tunes thrombotic responses.

• Why it matters: Influenza increases thrombotic risk, and while vRNA sensing by RIG-I is known elsewhere, platelet RIG-I signaling and its impact on clotting outcomes were unclear.
• What they did: Platelets from non-infected and influenza-infected patients were analyzed for RIG-I presence and function, then stimulated with influenza-derived vRNA to assess granule release, interferon signaling, MAVS signaling, pMLKL, and S100A10/S100A8/A9 release. In vivo, MAVS deficiency was tested during influenza using FeCl3-induced carotid occlusion and pulmonary vein analyses in mice.
• The result: RIG-I signaling increased pMLKL phosphorylation, oligomerization, and S100A10 surface presence without uniform α- or δ-granule release or interferon-pathway activation, and MAVS disruption increased thrombotic burden and shortened FeCl3 carotid occlusion times during influenza.

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