Disassembly of viral membranes by complement independent of channel formation.

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Abstract
The effects of the complement membrane attack complex (MAC), nystatin and melittin on the envelope of murine leukemia viruses were compared to determine if channel formation alone is sufficient to cause membranolysis. Nystatin is a channel former and mellitin is not, although both are hemolytic. Whereas MAC and melittin disintegrated the viral membrane, nystatin had no effect on morphology, integrity and infectivity of the virus. Incorporation of the antibiotic into the viral membranes was demonstrated by measurements of the characteristic fluorescence of nystatin in membranes and the dose-dependent increase in viral density after uptake of the antibiotic. The density of nystatin was measured to be 1.26-1.27 g/cm3. Proof for the formation of functional nystatin channels was obtained by light scattering measurements. Exposure of untreated virus to hypotonic conditions increased viral light scattering because of osmotic swelling but otherwise had no effect on the integrity of the virus. Nystatin channel formation abolished the light scattering change, showing that the antibiotic impaired the viral permeability barrier. Apparently, virolysis by MAC is not caused by channel formation and, in the absence of colloid-osmotic effects, channel formation by itself is not sufficient to disassemble a viral membrane.