Host-cell antigen potentiated by incomplete growth cycle of influenza virus.

Lysis of Ehrlich ascites tumor cells in mice was induced with the Hong Kong influenza A-strain HKH virus not previously adapted to the tumor. Despite high pathogenicity of HKH, mice not genetically resistant to the lethal action of myxoviruses survived the actue phase of oncolysis. Virus infection of tumor cells resulted in high titers of hemagglutinin with low infectivity which indicated incomplete virus growth. Serial passages of HKH in Ehrlich ascites tumors failed. HKH oncolysates induced solid antitumor immunity in several mouse strains, including those fully susceptible to the virus. The immunizing power of HKH oncolysates could be abolished by mouse antibody against egg-grown HKH (H3, N2) but not by antiserum raised aganist TUR virus (Havl, Nav3).