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Inhibition of Anatid herpesvirus replication by phosphonoacetate
Abstract:
Phosphonoacetate was found to be an effective inhibitor of the replication and cytopathic effects (CPE) associated with Anatid herpesvirus (AHV) infections in avian cells. In low multiplicity of infection (MOI) (10(-3) or less) infected Pekin duck and chicken fibroblast cultures, the dosage required for a 50% plaque reduction was approximately 20 microgram/ml. The amount of the inhibitor needed for complete prevention of CPE was found to be MOI dependent with up to 190 microgram/mL required at a MOI of 1.1. Delayed addition of phosphonoacetate to AHV-infected cultures resulted in differing CPE. When added before 25 h postinfection, the CPE were largely prevented. Added between 25 and 40 h postinfection, the CPE consisted of nonproductive, nonperforate focal areas containing viable and nonviable cells. The focal areas did not appreciably increase in size or number in the continued presence of phosphonoacetate, were chromophilic, and tended to be replaced by morphologically normal cells, provided the presence of phosphonoacetate was continued. Maintaining phosphonoacetate in the presence of infected cultures for periods of 7 days or longer resulted in curing and a complete loss of infections virus in the medium and in cell lysates.
Insights
Phosphonoacetate effectively inhibits Anatid herpesvirus (AHV) replication and cytopathic effects (CPE) in avian cells. Long-term treatment with phosphonoacetate can cure AHV infections, eliminating the virus from cultures.
Area of Science:
- Virology
- Antiviral Research
- Cell Biology
Background:
- Anatid herpesvirus (AHV) causes significant cytopathic effects (CPE) in avian cells.
- Viral replication and CPE necessitate effective antiviral interventions.
Purpose of the Study:
- To evaluate phosphonoacetate as an inhibitor of AHV replication and CPE.
- To determine the efficacy of phosphonoacetate in preventing and treating AHV infections in avian cell cultures.
Main Methods:
- Infection of Pekin duck and chicken fibroblast cultures with AHV at varying multiplicities of infection (MOI).
- Treatment of infected cultures with phosphonoacetate at different time points post-infection.
- Assessment of plaque reduction, CPE, viral load, and cell viability.
Main Results:
- Phosphonoacetate demonstrated dose-dependent inhibition of AHV replication and CPE.
- Complete prevention of CPE required higher phosphonoacetate concentrations at higher MOI.
- Delayed addition of phosphonoacetate modulated CPE, and prolonged treatment (≥7 days) led to viral clearance and cell recovery.
Conclusions:
- Phosphonoacetate is a potent inhibitor of Anatid herpesvirus.
- The timing and duration of phosphonoacetate treatment influence its therapeutic effect, with sustained application potentially leading to a cure.