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The genetically selected high antibody responder line of mice (HIII) for a natural immunogen were fully susceptible to mouse hepatitis virus 3 (MHV3) and the corresponding low antibody responder mice (LIII) were fully resistant, regardless of whether they were previously treated or not with the bacillus Calmette-Guérin (BCG). The resistance or susceptibility correlated with the virus growth in the peritoneum of mice. Peritoneal cells isolated from resistant mice released higher amounts of H2O2after phorbol myristate acetate (PMA) stimulation than susceptible mice. No spontaneous in vitroH2O2release by peritoneal exudate cells from HIIImice, shown to be mostly macrophages, were observed during the MHV3 infection, In contrast, the spontaneous in vitroH2O2release by these cells from MHV3-infected LIIImice increased gradually, reaching a maximal value 3 days after infection, and decreased in parallel to the virus clearance from the peritoneum. The BCG treatment primed the macrophages of HIIImice for the production of H2O2during the MHV3 infection, but did not confer resistance against the virus infection. The data obtained suggest that the acquired capability of macrophages to release H2O2does not participate in the anti-MHV3 activity or resistance against the MHV3 infection.