During passage in mice which had been vaccinated with the homologous, and with closely related strains of influenza virus, the passage strain developed a lessened susceptibility to the deleterious effects of the "immune" environment, concommittant with which was a developed capacity to evoke antibodies which reacted with earlier strains of virus—a capacity which was inapparent in the parent strain. However, the parent strain exhibited a relatively broad range of surface reactivity which was not apparent in the derived strain.
The data are interpreted to mean that the hereditary change resulted from spatial rearrangement and quantitative redistribution of antigens in the virus particle (in which the surface is viewed as being distinct from the inner bulk), and are viewed as enhancing the idea that influenza virus variation (i.e., "mutation") may result from a rearrangement of existing hereditary elements.
