Modulation of coronavirus-mediated cell fusion by homeostatic control of cholesterol and fatty acid metabolism
Cellular susceptibility to fusion mediated by murine coronavirus (mouse hepatitis virus, MHV strain A59) was separated into lipid-dependent and lipid-independent mechanisms with the use of subclones and selected mutants of mouse L-2 fibroblasts. Fusion-resistant L-2 cell mutants had similar cholesterol and fatty acid composition as did their fusion-susceptible parent subclone, and were presumably
