Virus infections transiently suppress pulmonary antibacterial defenses by causing dysfunctions in the alveolar macrophage phagocytic system. This impairment of pulmonary bactericidal activity is not associated in time with virus proliferation, but rather with the period of time of rapidly declining virus titers and the expression of the antiviral immune response in the lungs. This temporal relationship suggests that the impairment of pulmonary bactericidal activity might be secondary to the antiviral immune response rather than a direct effect of virus replication. Immune depletion of mice during the course of influenza virus pneumonia ameliorated the virus-induced bactericidal defect and prevented bacterial multiplication in the lungs. In contrast, immune reconstitution reestablished the alveolar macrophage phagocytic defect. These data indicate that virus-induced suppression of pulmonary antibacterial defenses may be, in part, immunologically mediated.