Interferon inhibits Sendai virus-induced cell fusion: an effect on cell membrane fluidity.

Abstract

Interferon can affect several cellular functions, in addition to its antiviral activity. Pretreatment of human cells with homologous interferon significantly inhibits cell fusion induced by Sendai virus and this refractory state is accompanied by a decrease in cell plasma membrane fluidity. Multinucleate cell formation induced by .beta.-propiolactone-inactivated Sendai virus in human fibroblast cells (a system in which fusion results from an interaction of the viral glycoprotein with the cell membrane) was inhibited by > 90% after addition of human interferon for 18-24 h. This inhibition could be neutralized by antiserum to interferon. Inhibitor studies with cycloheximide and actinomycin D clearly indicated that synthesis of protein and RNA is necessary to establish the resistant state. To determine whether the inhibition of Sendai virus-induced cell fusion resulted from interferon-induced changes at the cell plasma membrane, experiments were carried out using the fluorescence probe, 1,6-diphenyl-1,3,5-hexatriene, which is capable of sensing molecular motions in the hydrocarbon core of the bilayer structure. A significant decrease in the membrane fluidity of interferon-treated cells was observed. The inhibitory effect on Sendai virus-induced cell fusion observed in interferon-treated cells may result from an increased rigidity of the target cell membrane.