Severe Influenza A virus (IAV) infection is associated with endothelial dysfunction, inflammation, and coagulation abnormalities. However, the mechanisms linking endothelial inflammatory activation to thrombosis remain incompletely understood. We investigated whether Influenza A/H1N1 induces an immunothrombotic phenotype in human brain microvascular endothelial cells. We infected HBEC-5i cells with Influenza A/H1N1 pdm09. We assessed viral infection by RT-qPCR detection of matrix (M) transcripts and by immunoblotting for the M1 protein. We evaluated endothelial responses by measuring TNF-α expression and secretion, Tissue Factor (TF) expression, TF-dependent factor Xa generation, and responses to recombinant TNF-α and thrombin. H1N1 infection increased TNF-α expression and secretion and enhanced TF expression and functional activity, indicating acquisition of a procoagulant endothelial phenotype. Recombinant TNF-α reproduced infection-associated TF induction, whereas thrombin enhanced TNF-α production and TF activity, supporting reciprocal amplification between inflammatory and coagulation pathways. These findings support a TNF-α–TF–thrombin feed-forward signaling circuit linking endothelial inflammation and coagulation during H1N1 infection. Influenza A/H1N1 induces an immunothrombotic phenotype in human brain microvascular endothelial cells, identifying this signaling axis as a potential mechanistic target for influenza-associated vascular and thrombotic complications.