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Effect of tunicamycin on cell fusion induced by Mason-Pfizer monkey virus
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 has been carried out 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 micrograms of the drug per ml was tested. Furthermore, no significant effect on the extent of syncytium formation in rhesus monkey fetal lung cells was observed when the time of addition or duration of treatment with this inhibitor was varied. Nevertheless, tunicamycin was very effective in blocking glycosylation in rhesus cells since virions produced in the presence of this drug completely lacked gp70 and gp20, the two 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. These results indicate that glycosylation of the fusion-inducing product is not required for multinucleate cell formation induced by Mason Pfizer monkey virus.
Insights
Glycosylation is not required for Mason-Pfizer monkey virus-induced cell fusion. Even when tunicamycin blocked viral glycoprotein production, syncytium formation still occurred, indicating non-glycosylated products can mediate fusion.
Area of Science:
- Virology
- Cell Biology
Background:
- Mason-Pfizer monkey virus (MPMV), a D-type retrovirus, causes cell fusion (syncytium formation) in primate cells.
- The role of viral glycoproteins in this fusion process is not fully understood.
Purpose of the Study:
- To investigate whether a glycosylated product is responsible for the cell fusion property of MPMV.
- To determine if inhibiting glycosylation affects MPMV-induced syncytium formation.
Main Methods:
- Rhesus monkey fetal lung cells were infected with MPMV and treated with tunicamycin, a glycosylation inhibitor.
- Viral glycoproteins (gp70, gp20) and syncytium formation were assessed.
- Non-glycosylated virions were tested for infectivity and fusion capability.
Main Results:
- Tunicamycin treatment effectively blocked glycosylation of MPMV virions, eliminating gp70 and gp20.
- Despite the lack of glycosylation, tunicamycin did not inhibit cell fusion or syncytium formation.
- Non-glycosylated, noninfectious virions were produced in the presence of tunicamycin.
Conclusions:
- Glycosylation of viral products is not essential for Mason-Pfizer monkey virus-induced cell fusion.
- The fusion-inducing component of MPMV can function in a non-glycosylated form.