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A full-length murine 2-5A synthetase cDNA transfected in NIH-3T3 cells impairs EMCV but not VSV replication
E M Coccia1, G Romeo, A Nissim
1Laboratorio di Virologia, Istituto Superiore di Sanità, Rome, Italy.
Abstract:
Treatment of cells with interferons (IFNs) induces resistance to virus infection. The 2'-5'oligo A (2-5A) synthetase/RNase L is one of the pathways leading to translation inhibition induced by IFN treatment. A murine cDNA encoding the 43-kDa 2-5A synthetase was cloned and sequenced. NIH-3T3 cell clones transfected with this cDNA expressed the enzymatic activity to various extents and exhibited resistance to encephalomyocarditis virus (EMCV) but not to vesicular stomatitis virus replication. The specific resistance to EMCV can be attributed to 2-5A synthetase.
Insights
Interferon treatment confers virus resistance via the 2-5A synthetase pathway. This pathway specifically inhibits encephalomyocarditis virus replication in cells expressing the 2-5A synthetase enzyme.
Area of Science:
- Molecular Biology
- Virology
- Immunology
Background:
- Interferons (IFNs) are crucial for antiviral defense.
- The 2-5A synthetase/RNase L pathway is a key mechanism for IFN-induced translation inhibition and virus resistance.
Purpose of the Study:
- To clone and characterize the murine 2-5A synthetase.
- To investigate the role of 2-5A synthetase in conferring resistance to specific viral infections.
Main Methods:
- Cloning and sequencing of a murine 43-kDa 2-5A synthetase cDNA.
- Transfection of NIH-3T3 cells with the 2-5A synthetase cDNA.
- Assessing viral replication of encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV).
Main Results:
- Successful cloning and sequencing of the murine 2-5A synthetase cDNA.
- NIH-3T3 cell clones expressed varying levels of 2-5A synthetase enzymatic activity.
- Transfected cells showed specific resistance to EMCV replication, but not VSV replication.
Conclusions:
- The 2-5A synthetase enzyme is responsible for the observed specific resistance to EMCV.
- This study elucidates a specific antiviral mechanism mediated by 2-5A synthetase in response to interferon treatment.
