Related Experiment Videos
Sodium butyrate activates human immunodeficiency virus long terminal repeat--directed expression
C Bohan1, D York, A Srinivasan
1Division of Viral Diseases, Centers for Disease Control, Atlanta, GA 30333.
Biochemical and Biophysical Research Communications
|November 13, 1987
Summary
Sodium butyrate activates human immunodeficiency virus (HIV) long terminal repeat (LTR) expression in cell cultures. This finding aids in understanding how chemical agents affect HIV, using a pLTR-CAT plasmid model.
Area of Science:
- Molecular Biology
- Virology
- Biochemistry
Background:
- The human immunodeficiency virus (HIV) long terminal repeat (LTR) regulates viral gene expression.
- Understanding factors that modulate HIV LTR activity is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the impact of sodium butyrate on HIV LTR-directed gene expression.
- To establish a model system for evaluating chemical and biological agents' effects on HIV.
Main Methods:
- Construction of a chimeric plasmid (pLTR-CAT) fusing HIV LTR sequences to the chloramphenicol acetyltransferase (CAT) gene.
- Transient expression assays in transfected tissue culture cells to measure LTR activity.
Main Results:
- Sodium butyrate significantly activated pLTR-CAT expression in transfected cells.
- The activation by butyrate showed a linear dose-dependent response up to 8 mM.
- The magnitude of activation varied depending on the specific target promoters used.
Conclusions:
- Sodium butyrate can enhance HIV LTR-directed expression.
- The pLTR-CAT plasmid serves as a valuable model for studying the effects of various agents on HIV.
- Further research can utilize this model to identify novel therapeutic interventions targeting HIV gene expression.