Herpes Drug Doesn’t Lower Risk of HIV Infection
By Sandi Doughton, Seattle Times
Feb. 4–In another setback for AIDs research, Seattle scientists reported today that use of the drug acyclovir to treat people with genital herpes did not lower their risk of contracting HIV.
The findings tempered the hope that herpes medications might provide a cheap and easy way to slash transmission of HIV around the world.
“We were surprised and disappointed,” said Dr. Connie Celum, the University of Washington researcher who led the study of more than 3,000 herpes-infected people on three continents.
Infection with herpes simplex virus 2, the cause of most genital herpes, can double or even triple a person’s odds of contracting HIV. One of the most common sexually transmitted diseases worldwide, herpes often leads to recurring outbreaks of genital sores that are believed to provide a route for HIV to slip into the body.
So scientists had been optimistic that acyclovir, a generic drug that reduces herpes outbreaks, would also reduce the odds of HIV infection.
But 3.9 percent of those who received acyclovir in the clinical trail came down with HIV, roughly equivalent to the 3.3 percent infection rate in the control group who did not get the herpes drug. The trial was double-blind, which is considered the gold standard in research, because even the scientists don’t know which participants got the drug or a placebo until the results are tabulated.
The bad news comes a few months after a major AIDS vaccine trial, also led by Seattle scientists, was halted after hints that the drug might actually make people more likely to contract the disease. Two large studies of microbicides, gels that women insert in their vaginas to protect against HIV infections, were also stopped after it appeared the gels might increase vulnerability to the deadly virus.
Also today another group of researchers reported that circumcision, which has been shown to reduce men’s risk of HIV infection, provides no such benefit to the men’s female partners.
“It’s certainly discouraging to have several trials in a row that don’t have the hoped-for results,” said Celum, who presented the herpes results in Boston at the Fifteenth Conference on Retroviruses and Opportunistic Infections. But scientists can often learn as much from failures as successes, she added.
For example, it may be possible that inflammation lingers after a herpes outbreak — even outbreaks that aren’t noticeable to the infected person, Celum said. HIV can easily attach to immune system cells, called T-cell, that are present in inflamed tissues.
“It may be there’s more to it than just the herpes virus being present,” she said. “Maybe the immune response to the virus in the genital tract is important.”
The Seattle scientists are also conducting a small trial to see if higher doses of acyclovir will work better to cut down herpes outbreaks and viral shedding. The herpes-HIV trail used the standard dosage of 400 mg, twice a day.
The trials were conducted in Seattle, New York, San Francisco, Peru and several African nations. Participants in the United States and South America were herpes-infected men who have sex with men. Volunteers in Africa were herpes-infected women.
Sandi Doughton: 206-464-2491 or sdoughton@seattletimes.com
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