Abstract
We have developed a complementation assay, using transiently transfected COS cells, to facilitate a molecular analysis of the herpes simplex virus type 1 glycoprotein gH. When infected by a gH-null syncytial virus, COS cells expressing wild-type gH generate infectious progeny virions and form a syncytium with neighboring cells. By deletion and point mutagenesis, we have found particular residues in the gH cytoplasmic tail to be essential for generation of a syncytium but apparently dispensable for production of infectious virions. This study emphasizes the different requirements for cell-cell and cell-envelope fusion and demonstrates that changes in the non- syn locus UL22-gH can reverse the syncytial phenotype.
Original language | English (US) |
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Pages (from-to) | 6985-6993 |
Number of pages | 9 |
Journal | Journal of virology |
Volume | 68 |
Issue number | 11 |
DOIs | |
State | Published - Nov 1994 |
ASJC Scopus subject areas
- Microbiology
- Immunology
- Insect Science
- Virology