We show that during malaria, P. falciparum infection impairs serum bactericidal immunity to S. Typhimurium via altered complement C3 deposition on S. Typhimurium in addition to the impairment of the respiratory burst of phagocytes which was known before, providing a comprehensive explanation for the increased susceptibility to iNTS seen in children during malaria. This evidence concerns the gene C3 and malaria.