A patient with primary Sjögren's syndrome developed pulmonary embolism following infection with influenza A virus. IgM anti-cardiolipin autoantibodies (aCL) evolved two weeks after hospitalisation, synchronously with antibodies against influenza A. IgG aCL developed three weeks after hospitalization, peaked during the recovery period, and gradually declined to undetectable levels 12 months after admission. Antibodies against beta2 glycoprotein I were not detected. Our results assign a high likelihood to the hypothesis that influenza A virus caused the patient's thromboembolic disease as well as development of aCL. aCL may have contributed to tissue pathology by forming immune-complexes with cardiolipin and rheumatoid factor.