It is thought that SP-HUS results from desialylation of host cells by the pneumococcal neuraminidase, which result in the exposition of the Thomsen-Friedenreich antigen (TF) in erythrocytes, platelets and glomeruli and its subsequent interaction with natural anti-TF antibodies (6, 7), and/or in reduced protection of host cells against autologous complement (8, 9). The gene discussed is TF; the disease is hemolytic-uremic syndrome.