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J Virol. 1979 June; 30(3): 883-890
1 Division of Biology, Kansas State University, Manhattan Kansas 66506
2 Department of Medicine, Northwestern University Medical School and Veterans Administration Lakeside Hospital, Chicago, Illinois 60611
3 Department of Pathology (Neuropathology), Northwestern University Medical School and Veterans Administration Lakeside Hospital, Chicago, Illinois 60611
ABSTRACT
A temperature sensitive mutant of vesicular stomatitis virus which does not mature properly when grown at 39°C promoted extensive fusion of murine neuroblastoma cells at this nonpermissive temperature. Polykaryocytes apparently formed as a result of fusion from within the cells that requires low doses of infectious virions for its promotion and is dependent on viral protein synthesis. Although 90% of infected N-18 neuroblastoma cells were fused by 15 h after infection, larger polykaryocytes continued to form, leading to an average of 28 nuclei per polykaryocyte as a result of polykaryocytes fusing to each other. Two neuroblastoma cell lines have been observed to undergo fusion, whereas three other cell lines (BHK-21, CHO, and 3T3) were incapable of forming polykaryocytes, suggesting that nervous system-derived cells are particularly susceptible to vesicular stomatitis virus-induced fusion. Although the normal assembly of the protein components of this virus is deficient at 39°C, the G glycoprotein was inserted into the infected cell membranes at this temperature. Two lines of evidence suggest that the expression of G at the cell surface promotes this polykaryocyte formation: (i) inhibition of glycosylation, which may be involved in the migration of the G protein to the cellular plasma membranes, will inhibit the cell fusion reaction; (ii) addition of antiserum, directed toward the purified G glycoprotein, will also inhibit cell fusion.
Contribution no. 79-152-j, Kansas Agricultural Experiment Station, Kansas State University, Manhattan, KS 66506.
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