Could You One Day Wine and Dine Your Cold Sores -- to Death?

From the WebMD Archives

Sept. 19, 2000 (Toronto) -- A chemical related to an active ingredient of red wine stops the herpes virus in its tracks -- in the lab. If the compound, or its relatives, pan out in animal and human studies, it could one day offer an alternative to treat genital herpes and cold sores that resist the most common antiherpes drug, according to results presented here at a meeting of infectious disease specialists.

The compound, called stil-5, cripples the virus using a different strategy than the most common antiherpes drug, Zovirax (acyclovir). That means that it might work on virus strains that have developed resistance to current treatments.

Stil-5 almost completely stopped the virus from reproducing, co-author Mathew Lesniewski, tells WebMD. Lesniewski is a graduate student at Kent State University in Kent, Ohio. He worked with project leader John Docherty, PhD, of Northeastern Ohio Universities College of Medicine, and chemist Chun-che Tsai, PhD, of Kent State.

For years, people who suffered from genital herpes and cold sores had no recourse when the virus attacked. In the 1980s, drug researchers developed Zovirax, which stops the herpes viruses that cause these sores from reproducing, and recently other effective drugs have made it to the market. But herpes strains that withstand these drugs have begun to appear, prompting researchers to begin looking for alternatives.

"It's kind of a foot race, and you've got to stay ahead of the bug," Lesniewski says.

Last year, the Ohio team found that a compound from red wine called resveratrol blocks the herpes virus that causes cold sores from reproducing. Because resveratrol worked too weakly to make a good drug, the researchers began searching for chemical relatives that might be more potent.

The researchers then developed five related compounds and began testing them on the herpes virus. Of the five compounds, only stil-5 worked at low concentrations, Lesniewski says.

Further tests by the team showed that stil-5 did not kill cells and that it might be working by blocking a protein that sets virus reproduction in motion.

Next, the researchers hope to make related compounds that are even more potent than stil-5. "This will be our jumping-off point," Lesniewski tells WebMD.

The work is "intriguing," says Wayne Cheney, PhD, of ICN Pharmaceuticals in Costa Mesa, Calif. But he emphasizes that there's a long way to go, and it has to work as well as Zovirax. "If it's as potent as that, it would be great," he says. "Otherwise, it's not going to go."