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Herpes simplex virus ribonucleotide reductase mutants are hypersensitive to acyclovir.
D M Coen1, D J Goldstein, S K Weller
1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115.
Antimicrobial Agents and Chemotherapy
|August 1, 1989
Summary
Herpes simplex virus mutants lacking ribonucleotide reductase showed increased sensitivity to antiviral drugs like acyclovir. This finding is crucial for understanding drug resistance and developing new therapies targeting viral ribonucleotide reductase.
Area of Science:
- Virology
- Molecular Biology
- Drug Discovery
Background:
- Herpes simplex virus (HSV) relies on its own enzymes for DNA replication.
- Ribonucleotide reductase is essential for providing building blocks for viral DNA synthesis.
Purpose of the Study:
- To investigate the role of HSV-encoded ribonucleotide reductase in antiviral drug sensitivity.
- To explore the implications of inhibiting viral ribonucleotide reductase for drug resistance and development.
Main Methods:
- Generation and characterization of HSV mutants deficient in ribonucleotide reductase activity.
- Assessment of mutant sensitivity to antiviral drugs including acyclovir, aphidicolin, and phosphonoacetic acid.
Main Results:
- Mutants defective in viral ribonucleotide reductase displayed significant hypersensitivity to acyclovir and aphidicolin.
- A lesser degree of hypersensitivity was observed with phosphonoacetic acid.
Conclusions:
- Viral ribonucleotide reductase activity is a key factor in determining HSV sensitivity to certain antiviral drugs.
- Inhibiting viral ribonucleotide reductase may be a viable strategy to overcome acyclovir resistance and enhance antiviral efficacy.