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Acylovir in oral and ganglionic herpes simplex virus infections
Abstract:
The local and trigeminal ganglionic therapeutic efficacy of two topical and systemic antiviral drugs was studied in mouse lips inoculated with herpes simplex virus type 1 after thermal injury. Application of topical 3% acylovir (acycloguanosine) ointment three times daily for four days completely blocked the replication of virus in the lips, and the healing process was greatly accelerated compared with that in placebo-treated infected controls. However, neither the healing process nor the viral replication was influenced by similar therapy with 3% vidarabine ointment. When given systemically for four days, starting one day after inoculation, acyclovir (40-60 mg/kg per day) and vidarabine (50 mg/kg per day) significantly reduced the clinical manifestations on the lips and viral titers of cultures obtained from the lips. Establishment of viral latency in the trigeminal ganglion was significnatly inhibited by systemic acyclovir (60 mg/kg per day), whereas systemic vidarabine (50 mg/kg per day) was ineffective. These data suggest that acyclovir may be one of the most promising antiviral agents for the management of oral herpes viral infections and trigeminal ganglionic latency of virus as demonstrated in the mouse model.
Insights
Topical acyclovir (acycloguanosine) ointment effectively treated herpes simplex virus type 1 in mouse lips. Systemic acyclovir also reduced oral herpes symptoms and prevented viral latency in the trigeminal ganglion.
Area of Science:
- Virology
- Pharmacology
- Immunology
Background:
- Herpes simplex virus type 1 (HSV-1) causes oral herpes infections.
- Thermal injury can exacerbate HSV-1 infections.
- Antiviral therapies aim to reduce viral replication and prevent latency.
Purpose of the Study:
- To evaluate the therapeutic efficacy of topical and systemic acyclovir (acycloguanosine) and vidarabine for HSV-1 infections in mouse lips.
- To assess the drugs' impact on viral replication, lesion healing, and trigeminal ganglion latency.
Main Methods:
- Mice with HSV-1 inoculated lips after thermal injury were treated with topical or systemic acyclovir or vidarabine.
- Viral replication, lesion healing, and viral titers were measured.
- Establishment of viral latency in the trigeminal ganglion was assessed.
Main Results:
- Topical acyclovir completely blocked viral replication and accelerated healing.
- Systemic acyclovir reduced clinical manifestations and viral titers.
- Systemic acyclovir significantly inhibited viral latency in the trigeminal ganglion, while vidarabine was ineffective.
Conclusions:
- Acyclovir demonstrates significant therapeutic potential for managing oral herpes infections.
- Acyclovir effectively reduces viral replication, promotes healing, and inhibits HSV-1 latency in the trigeminal ganglion.
- These findings support acyclovir as a promising agent for oral herpes management.