Swiss mice were intranasally infected with influenza A2 virus and treated with urethan in order to detect whether the joint action of the two agents would enhance the development of lung tumors. The average number per mouse of the typical lesions induced by the two treatments together with their location, their histological and histochemical characteristics and the percentage of death in the different groups of animals were recorded. Results indicated that 51.7 % of the mice infected with influenza virus and treated with urethan had both bronchial dysplastic lesions due to influenza virus, and tumors induced by urethan. In this group the number of tumors was smaller than in the mice treated with the carcinogen only and no invasive pulmonary carcinomas were observed. The dysplastic lesions caused by influenza A2 virus as well as the lung adenomas induced by urethan maintained their typical histological and histochemical characteristics even when occurring in a close position. The failure of urethan to enhance the induction of lung tumors in mice exposed to influenzal infection might be ascribed to the different primary sites of response of the pulmonary tissue to the two agents, i.e. the bronchial epithelium for influenza virus and the alveolar epithelium for urethan.
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