Treatment of experimental latent herpes simplex virus infections with acyclovir and other antiviral compounds.
Acyclovir can prevent the establishment of latent herpes simplex virus (HSV) in sensory ganglia by early treatment of the primary infection in experimental animals. A delayed treatment may reduce the number of neurons that eventually become latently infected. Acyclovir can prevent virus reactivation in explant cultures of latently infected ganglia, experimentally induced recurrences of latently infected animals, and immunosuppressed patients. This effect is dependent on the continuous presence of the drug in the explant culture medium or organism. The treatment of recurrent lesions with acyclovir reduces the severity of the episode and may also prevent reinfection of ganglia, if this should be common in the maintenance of latency. It might be possible to eradicate a latent HSV, if conditions were created in which drugs such as acyclovir, activated by the virus-induced thymidine kinase, could interact with the enzyme before the assembly of mature virions.
D000212:Acyclovir; D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use*; D046508:Culture Techniques; D017245:Foscarnet; D005724:Ganglia / Q000382:microbiology*; D006147:Guanine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D006561:Herpes Simplex / Q000188:drug therapy* / Q000382:microbiology; D051379:Mice; D009474:Neurons / Q000382:microbiology; D010746:Phosphonoacetic Acid / Q000031:analogs & derivatives / Q000627:therapeutic use; D018139:Simplexvirus / Q000502:physiology; D013997:Time Factors
D000998:Antiviral Agents; D017245:Foscarnet; D006147:Guanine; D010746:Phosphonoacetic Acid; D000212:Acyclovir