New therapies developed for herpes simplex virus
Resistant strains are appearing
When it comes to viruses, HIV gets most of the press these days. But researchers are looking into new therapies for several other viral pathogens, including herpes simplex, also known as genital herpes.
Often overshadowed by HIV, herpes simplex virus, or HSV, affects millions more people than its more notorious cousin, manifesting either as a genital lesion, technically known as HSV-2, or as a "cold sore," known as HSV-1. To date, the most effective treatment for herpes simplex infections has been acyclovir.
Now resistant strains of HSV are beginning to appear. Also, acyclovir has no affect on asymptomatic viral shedding, that period during which the virus remains potentially active but latent.
6 compounds now under study
Among the new compounds under study for HSV infections:
• n-Docosanol: This long-chain alcohol (it has 22 carbons) not only works to heal genital herpes lesions when applied topically, but it also helps heal lesions from Kaposi’s sarcoma a type of cancer common in AIDS patients. It’s currently undergoing clinical trials.
• Brivudin: Studies show this new drug works best when it’s dosed about five hours post-infection, the time when viral thymidine kinase (TK) activity hits its peak. Brivudin inhibits viral TK and works even better when dosed with acyclovir.
• Gigartina skottsbergii: Not your average antiviral, this red seaweed collected in Argentina, is said by researchers in Buenos Aires to contain a carrageenan that prevents the herpes simplex virus from adhering to cells.
No place to stick
• Nonionic detergents: The idea again is to prevent viral adhesion to cells. One of the more promising compounds in this department is Triton X-165. One of the least promising is Tween 20. The problem with the latter compound and many of these detergents in general is their high toxicity to normal cells.
• Ro 32-1520 and 32-2313: Steering back to conventional medicine, these compounds, taken orally, attack HSV while it hides by inhibiting viral TK. Viral TK is thought to be necessary to spur latent virus into an active state. Once the herpes virus begins replicating, however, it uses host cellular TK to reproduce.
• Herpes vaccine: Someday perhaps soon children will not only get vaccinations against diptheria, pertussis, and tetanus, but also against herpes. Researchers have identified a potential candidate called RAV 9395. This compound looks exactly like the herpes simplex virus, except that four genes which contribute to virulence have been deleted. Tests in guinea pigs show the vaccine is protective and well-tolerated.
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