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Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
Gene-specific transactivation by herpes simplex virus type 1 alpha protein ICP27
1Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Journal of Virology
|October 1, 1988
Summary
Herpes simplex virus type 1 (HSV-1) alpha protein ICP27 specifically boosts glycoprotein B (gB) expression. This suggests multiple viral factors are needed for full HSV-1 gene expression during infection.
Area of Science:
- Virology
- Molecular Biology
- Gene Regulation
Background:
- Herpes simplex virus type 1 (HSV-1) utilizes immediate-early (alpha) proteins to control gene expression during replication.
- Understanding these regulatory mechanisms is crucial for comprehending viral pathogenesis.
Purpose of the Study:
- To investigate the specific role of the HSV-1 alpha protein ICP27 in regulating the expression of viral genes, particularly glycoprotein B (gB).
- To elucidate the mechanism by which ICP27 influences gB gene expression.
Main Methods:
- Utilized temperature-sensitive HSV-1 mutants to assess protein synthesis under varying conditions.
- Constructed a plasmid to fuse the gB promoter-regulatory region to the chloramphenicol acetyltransferase (CAT) reporter gene.
- Analyzed CAT gene expression and transcript levels in response to ICP27.
Main Results:
- ICP27 significantly enhanced gB expression, demonstrating a marked dependence of gB on functional ICP27.
- ICP27 induction of CAT activity correlated with increased transcription initiation from the gB promoter.
- ICP27's transactivating activity was specific to the gB promoter-regulatory region, mapping to sequences within 175 bp upstream and 41 bp downstream of the transcription start site.
- ICP27 also affected the electrophoretic mobility of the alpha protein ICP4.
Conclusions:
- ICP27 is a key viral transactivator that specifically stimulates the expression of the HSV-1 gB gene.
- The findings suggest that optimal expression of gB and potentially other viral genes requires the synergistic action of multiple viral transactivators during HSV-1 infection.
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