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Acyclovir in mouse cytomegalovirus infections.
The American Journal of Medicine
|July 20, 1982
Summary
Mouse cytomegalovirus (MCMV) shows surprising sensitivity to acyclovir, even without encoding thymidine kinase. This suggests MCMV DNA polymerase is the drug's target, offering insights into antiviral therapies.
Area of Science:
- Virology
- Antiviral Drug Research
Background:
- Acyclovir efficacy in herpes viruses typically requires virus-encoded thymidine kinase.
- Mouse cytomegalovirus (MCMV) lacks thymidine kinase but exhibits high sensitivity to acyclovir.
Purpose of the Study:
- To investigate the mechanism of acyclovir's antiviral activity against MCMV.
- To identify the target of acyclovir in MCMV infections.
Main Methods:
- In vitro and in vivo studies of MCMV susceptibility to acyclovir.
- Isolation and characterization of acyclovir-resistant MCMV mutants.
- Analysis of drug resistance markers, including co-resistance with phosphonoacetic acid.
Main Results:
- MCMV is sensitive to acyclovir independent of thymidine kinase activity.
- Acyclovir's action does not require a thymidine phosphorylation pathway.
- Resistant MCMV mutants indicate inhibition of viral replication, with evidence pointing to MCMV DNA polymerase as the drug's target.
Conclusions:
- Acyclovir targets MCMV DNA polymerase, bypassing the need for viral thymidine kinase.
- This finding has implications for treating herpesvirus infections where viruses lack thymidine kinase, such as human cytomegalovirus and Epstein-Barr virus.