Altered sensitivity to antiviral drugs of herpes simplex virus isolates from a patient with the acquired immunodeficiency syndrome

Human immunodeficiency virus (HIV) is the causative agent of AIDS. Individuals with HIV infection have suppressed immune systems and are at greater risk for developing opportunistic infections. Herpes simplex virus (HSV) is a common infection among patients with HIV, and acyclovir is the usual treatment for HSV infection in these patients. For acyclovir to work, it must be activated by an enzyme called thymidine kinase (TK), which is present in the virus. However, some mutant strains of HSV lack the TK enzyme, and thus are not killed by acyclovir. These strains of HSV are called acyclovir-resistant. Acyclovir-resistant HSV type 2 (HSV-2) was isolated from a 24-year-old female patient with AIDS. The patient had no prior history of intravenous drug use, blood transfusions or herpes genitalis (genital herpes). She was treated with acyclovir, intermittently, for five months. During the initial stages of acyclovir therapy the genital lesions responded to the treatment, but did not heal completely. When HSV-2 was isolated from the patient and grown in culture, the combination of acyclovir and interferon reduced viral replication by greater than 97 percent. However, when administered to the patient, the combination of acyclovir and interferon only resulted in partial clinical improvement. Intravenous treatment with foscarnet for 10 to 12 days controlled severe ulceration of the lesions, but clinical improvement only lasted for 6 months. When HSV-2 infection recurred, the HSV-2 was resistant to both acyclovir and foscarnet. (Consumer Summary produced by Reliance Medical Information, Inc.)