Effect of tunicamycin on cell fusion induced by Mason-Pfizer monkey virus

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Abstract
Mason-Pfizer monkey virus, a D-type retrovirus, has been shown to induce multinucleate cell (syncytium) formation or cell fusion in several normal primate cells. A series of experiments was conducted to examine whether a glycosylated fusion-inducing product is responsible for this biological property of Mason-Pfizer monkey virus. Treatment of rhesus monkey fetal lung cells with different concentrations of tunicamycin, a potent inhibitor of glycosylation, during infection with Mason-Pfizer monkey virus had no effect on cell fusion even though up to 5 .mu.g /ml of the drug was tested. No significant effect on the extent of syncytium formation in rhesus monkey fetal cells was observed when the time of addition or duration of treatment with this inhibitor was varied. Tunicamycin was very effective in blocking glycosylation in rhesus cells since virions produced in the presence of this drug completley lacked gp70 and gp20, the 2 structural glycoproteins of Mason-Pfizer monkey virus. These non-glycosylated virus particles produced in the presence of tunicamycin were noninfectious as determined by a protein A binding assay and were unable to induce syncytium formation when assayed on rhesus cells. Glycosylation of the infusion-inducing product may not be required for multinucleate cell formation induced by Mason-Pfizer monkey virus.