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Vesicular stomatitis virus (VSV) induces polykaryocytes in rat embryonic fibroblasts transformed by the Prague strain of Rous sarcoma virus (XC cells). The cell fusion requires the uncoating of the virus in the cell, the synthesis of normally structured G and M proteins and their incorporation into the cell membrane. The synthesis of fully infectious virus is unnecessary. In addition to these antigens, a special yet undefined constitution of the host membrane is also important. With thermosensitive mutants non-defective for G and M antigens, cell fusion is much more extensive at the non-permissive temperature (39-6 degrees C) than at the permissive one (31 degrees C). The importance of these two antigens is also shown using rifampicin-sensitive mutants. We postulate that these two antigens induce in the cell membrane an imbalance in the distribution of phospholipids which then diffuse through membrane junctions to surrounding cells, provoking thereafter the cell fusion.

Mechanism of Polykaryocyte Induction by Vesicular Stomatitis Virus in Rat XC Cells