Cyclophosphamide was found to convert the mild Sendai virus infection of mice into a serious and sometimes fatal pneumonic illness, which appeared to be due to the failure of the mice to rid themselves of the infecting virus. The drug was shown to reduce the numbers of circulating white blood cells, to prevent the development of the mononuclear infiltration in the infected lung and to depress antibody production. It produced an initial depression of interferon production, but high concentrations of interferon were found in the lung during the late stages of the infection.

The significance of these findings is discussed in relation to the mechanisms of termination of virus infections and to the potential risk of respiratory disease during immunosuppressant therapy.


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