Results
Pathology and immunohistochemistry.
Varying degrees of degeneration and necrosis of respiratory epithelium with accompanying fibrin and neutrophils were present in trachea, bronchi, and bronchioles of the virus-infected mice. Necrotizing bronchitis was most frequent in mice receiving the wild-type WSN virus and occasionally was severe. Lungs had peribronchial alveolitis characterized by intraalveolar serofibrinous exudate, erythrocytes, and neutriphils, and increased alveolar macrophages. A mild to moderate bronchointerstitial pattern of pneumonia was frequent in 1918 NS A and 1918 NS B virus groups, but in the the WSN group, mice had diffuse severe interstitial pneumonia that affected entire lung lobes. Influenza nucleoprotein was demonstrated most consistently in mice inoculated with the transfectant virus and in degenerating or necrotic respiratory epithelium of trachea, bronchi, and bronchioles, and associated lumenal debris. Nucleoprotein was common in alveolar macrophages and epithelium of mice in transfectant groups. In general, the severity of lesions and amount of influenza viral antigen in the respiratory tract was greater for mice in the wild-type WSN group than either the 1918 NS A or 1918 NS B virus groups (Table 1). Mice inoculated with wild-type WSN, 1918 NS A, and 1918 NS B viruses lacked lesions in organs outside of the respiratory tract; i.e., brain, kidney, spleen, thymus, and liver. Lesions and viral antigen were absent from all tissues of the PBS sham control mice.