Establishment of aspergillosis is depending first, upon the survival of the conidia of Aspergillus fumigatus in the lung following up their recognition and phagocytosis by the cells of the host innate immunity and second, the exit from dormancy and germination of these eonidia in the lung environment.Reactive oxygen species (ROS) produced by phagocytic cells have been reported as being essential in the killing of A.fumigatus.Scavenging ROS enzymes such as SODs that detoxify superoxide anions, the initial precursor of ROS, and catalases that reduce H202 could be putative virulence factors for this opportunistic pathogen.Four genes encoding putative superoxide dismutases and three genes coding for catalases have been identified in the A.fumigatus genome.Single and multiple mutants were constructed.Catalase mutants had an increased sensitivity to hydrogen peroxide.The SOD1 and SOD2 mutant strains showed a growth inhibition at high temperature and hypersensitivity to menadione whereas the sod3 mutant had only a slight growth delay at high temperature.Multiple mutations have only an additive effect on the mutant phenoptype.The triple mutant was characterized by the highest sensitivity to menadione and to phagocytic reactions in the immunocompetent host.In spite of these phenotypes, no significant virulence difference was observed between the sodl sod2 sod3 triple mutant and wild type parental strain in experimental murine aspergillosis models.