A domain of murine retrovirus surface protein gp70 mediates cell fusion, as shown in a novel SC-1 cell fusion system

Virus-induced cell fusion of the fusion-from-without type was observed in SC-1 cells infected with Moloney murine leukemia virus when grown in NIH 3T3 cells. Replication-competent virus mutants with altered surface protein gp7O were examined. Fusion mutations were found in the proline-rich region of gp7O. They acted on a step after binding and before or during endocytosis. The fusion mutants had an altered gp7O isomer pattern, presumably caused by different glycosylation. Other mutants with deleted glycans were analyzed, and some which also showed defective fusion were found. The interrelationship of the proline-rich region, glycosylation, and fusion is discussed. Enveloped viruses enter cells by membrane fusion. This occurs either by plasma membrane fusion, as seen for Sendai virus (22, 32) and human immunodeficiency virus (HIV) (39), or by fusion with the membrane of acidic vesicles after endocytosis, as seen for ecotropic murine leukemia virus (MLV) (3, 24) and influenza virus (22). One aspect of membrane fusion is virus-mediated cell fusion (32). Two (or more cells) fuse to form a syncytium. This i