Antimetabolite drug therapy in herpes simplex.

Idoxuridine (IDU) and adenine arabinoside (Ara-A) are less than ideal drugs for the treatment of herpes because of toxicity, only partial efficacy with initial dendritic ulcers, and insufficient antiviral activity to prevent occasional epithelial breakthrough. Trifluorothymidine (TFT), soon to be released by the FDA for general use, appears to be more effective, curing 97% of ulcers in two weeks, and healing large ameboid ulcers more rapidly. Acycloguanosine, in combination with Ara-A, virtually eliminates stromal disease in rabbit eyes. A major advantage of this drug is its apparent lack of systemic toxicity due to its ability to interfere with the replication of virus-infected cells while not harming normal cells. Acycloguanosine should be available as an orally active, highly effective antiviral agent that can be given on an outpatient basis to treat deep infections. A new approach to the prevention of herpes recurrence involves the recognition that some isolates of herpes are mild or avirulent. Initial infection with avirulent virus may protect against virulent infection and yet may not cause disease. If such differences in virulence can be correlated with biochemical differences among the strains, prevention and treatment of herpes may be possible through manipulation of these metabolic pathways or immunization with avirulent virus.