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. 2026 Sep 14;16:1827915. doi: 10.3389/fcimb.2026.1827915

Figure 4.

Multi-panel scientific illustration showing the interaction between SFTSV (Severe Fever with Thrombocytopenia Syndrome Virus) and platelets, including explanatory legends, mechanisms of platelet activation, types of cell death (apoptosis, autophagy, pyrolysis, necroptosis), pathways leading to thrombocytopenia, viral effects on neutrophil activation, aggregation, and signaling pathways (PI3-AKT, RAP1, Ca signaling) involved in platelet function. Central diagram highlights SFTSV-platelet interaction surrounded by related biological processes and pathways.

SFTSV interaction with platelets. (A) Interaction between SFTSV Gn/Gc and Circulating Platelets. (B) Platelet Death Pathway. (C) SFTSV Infection Alters Platelet Function, Primarily by Regulating the Viral Life Cycle, Mediating Neutrophil Activation, Participating in Type I Interferon Release, and Influencing Platelet Aggregation, Adhesion, and Thrombus Formation. (D) SFTSV induces platelet activation and apoptosis via the ROS-MAPK pathway, simultaneously upregulating Bax/Bak expression and altering platelet membrane potential, leading to thrombocytopenia. (E) SFTSV interacts with platelets to downregulate transcription levels of genes associated with P13- AKT, RAP1, and Ca signaling pathways, thereby inhibiting platelet activation.