Altered interaction between Sendai virus and a Chinese hamster cell mutant with defective cholesterol synthesis.

An amphotericin B-resistant mutant (AMBr-1) isolated from the Chinese hamster V79 cell line is defective in a pathway for sterol synthesis and contains a much reduced free cholesterol level as compared with the parental V79. The character of the plasma membrane of AMBr-1 was compared with that of V79 by measuring the fusion with the envelope of the Sendai virus and also by measuring membrane fluidity: AMBr-1 was found to be more sensitive to Sendai virus-induced cytolysis than V79. Both assays for membrane-permeability change and electron spin resonance (ESR) study showed an enhanced response to the fusion between viral envelope and plasma membrane in AMBr-1 cells. Measurement of the fluorescence polarization for 1,6-diphenyl-1,3,5-hexatriene suggested that the membrane of AMBr-1 was more fluid than that of V79. This aberrant nature of the cell membrane of AMBr-1 might be caused by the altered membranous sterol content.