Deletion of the VP16 open reading frame of herpes simplex virus type 1
| Autor: | S K Durham, J L Resnick, S P Weinheimer, Donald R. O'Boyle, B A Boyd |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
DNA Replication
viruses Immunoblotting Molecular Sequence Data Immunology Mutant Biology Virus Replication medicine.disease_cause Microbiology Virus Open Reading Frames Viral Proteins Virology medicine Animals Simplexvirus Amino Acid Sequence Vero Cells Alleles Cell Line Transformed Recombination Genetic Herpes simplex virus protein vmw65 Mutation Expression vector biochemical phenomena metabolism and nutrition Molecular biology Blotting Southern Herpes simplex virus Viral replication Virion assembly Insect Science DNA Viral Mutagenesis Site-Directed Trans-Activators Research Article |
| Zdroj: | Journal of Virology. 66:258-269 |
| ISSN: | 1098-5514 0022-538X |
| DOI: | 10.1128/jvi.66.1.258-269.1992 |
| Popis: | VP16 (also called Vmw65 and alpha TIF) is a structural protein of herpes simplex virus type 1 (HSV-1) that trans-induces HSV-1 immediate-early gene transcription. This report describes an HSV-1 VP16 deletion mutant that was constructed and propagated in a cell line transformed with a VP16 expression vector. The VP16 deletion mutant replicated like wild-type HSV-1 during infection of the VP16-expressing cell line. Deletion mutant virions propagated in this cell line contained wild-type, cell-derived VP16 protein that was recruited during virion assembly and was functional for immediate-early gene trans-induction. The mutant failed to replicate during subsequent infection of cells that do not express VP16, as determined in plaque assays and single-step replication assays. The deletion mutant induced nearly normal levels of viral DNA synthesis and capsid production during these infections, but it induced slightly lower levels of viral DNA encapsidation and appeared by transmission electron microscopy to be defective in further steps of virion maturation. A genetic revertant of the deletion mutant that was restored for VP16-coding sequences exhibited fully wild-type replication properties in both VP16-expressing and nonexpressing cells. The absence of VP16 protein synthesis at late times of HSV-1 infection prevents the production of infectious progeny virus and correlates with a profound defect in HSV-1 particle assembly. |
| Databáze: | OpenAIRE |
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