Studies on virus-induced cell fusion. Progress report, August 1, 1977--June 30, 1978
We have previously postulated that wild-type Herpes Simplex Virus type I (HSV-1) infections are characterized by the presence of a fusion factor and a fusion inhibitor activity. The fusion inhibitor presumably is dominant so that a small fraction of cells fuse in a typical wild-type infection. Furthermore, the syn mutants isolated in our laboratory are thought to cause extensive cell fusion because the production of active fusion inhibitor in cell membranes is delayed. If mutations existed that altered both the fusion factor and fusion inhibitor activity then separate viruses containing these two mutations might be able to complement each other, each supplying the defective gene product missing in the other virus. This would produce a wild type and not a syncytial mutant response. Complementation tests between two viruses, tsB5 and syn 20, which are thought to contain defects in the production of active fusion factor and fusion inhibitor activity, respectively, were done. A wild-type response was observed indicating that the mutations affecting fusion were in two separate genes.
- Research Organization:
- Pennsylvania State Univ., University Park, PA (United States)
- DOE Contract Number:
- EY-76-S-02-3419
- OSTI ID:
- 6641713
- Report Number(s):
- COO-3419-19
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
HERPES SIMPLEX
INFECTIVITY
BIOCHEMICAL REACTION KINETICS
CELL MEMBRANES
GLUCOPROTEINS
MOLECULAR BIOLOGY
MUTANTS
CARBOHYDRATES
CELL CONSTITUENTS
DISEASES
INFECTIOUS DISEASES
KINETICS
MEMBRANES
ORGANIC COMPOUNDS
PROTEINS
REACTION KINETICS
SACCHARIDES
SKIN DISEASES
550200* - Biochemistry