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A vaccine for genital herpes has long eluded scientists. But now the first sign of a possible breakthrough has been offered by an international team of scientists from SmithKline Beecham and the University of Utah at the 40th Interscience Conference on Antimicrobial Agents & Chemotherapy (ICAAC) in Toronto.
The researchers' data on 2,714 patients showed the experimental vaccine was 73% effective at preventing herpes disease in high-risk populations of women who had previously never been exposed to any form of herpes. "For the first time ever, we have a grip on the herpes virus," said Dr. Spotswood Spruance, a microbiologist at the University of Utah School of Medicine and one of the trial's leading investigators.
Although the news was hopeful, Spruance emphasized the need for further studies. For example, researchers don't fully understand why the vaccine works only in women and not in men. Nor can they explain why only a specific group of women responded to the treatment. Women who had previously been exposed to the strain of herpes that causes cold sores, Herpes Simplex Virus 1, weren't significantly protected against the genital strain. Spruance noted that this discrepancy raises concerns about the vaccine's usefulness, since almost everyone is exposed to HSV1 at a very young age.
MORE HIV-SUSCEPTIBLE. The data is currently under review by the U.S. Food & Drug Administration. Spruance expects that further studies will be required before the drug is approved and that it will be several years before it's on the market.
Genital herpes, caused by the Herpes Simplex Virus 2 (HSV2), is a severe public-health problem in many countries, including the U.S., where some 500,000 new cases arise annually, according to the Centers for Disease Control in Atlanta. Symptoms include painful lesions in the genital area, itching, and burning. In rare cases, the virus spreads to internal organs, including the brain and spleen, and then is nearly always fatal. A person infected with genital herpes, like many other sexually transmitted diseases, is much more susceptible to HIV, the virus that causes AIDS.
There's no cure for herpes. Medication can control outbreaks, but small levels of the virus always remain in the body. The lack of a cure has spurred intense competition among researchers at universities and pharmaceutical companies to come up with a vaccine.
POWERFUL MOLECULE. Scientists at SmithKline realized from the start that for a vaccine to be effective, it had to contain a powerful activator compound, or adjuvant, capable of revving up the cell-killing functions of certain immune cells. So they included a molecule, SBAS4, that had been shown to boost animals' and humans' immune systems. SmithKline's use of SBAS4 was one of the critical reasons its vaccine succeeded.
To test the effectiveness of their drug, the researchers conducted two clinical trials, immunizing 2,714 men and women at high risk for developing herpes. The researchers defined high-risk candidates as people with a regular sexual partner with herpes. Participants were vaccinated with either the test therapy or a placebo at the start of the trial, and then again at three months and at six months. Nineteen months later, doctors examined the test group for signs of herpes or significant protection against the infection.
In both studies, only women who had never been exposed to either HSV1 or HSV2 were protected by the vaccine. Dr. Gary Dubin, director of the SmithKline Vaccine Efficacy study group in Belgium, noted that 10% of the women taking the placebo developed symptoms of genital herpes, while only 2.9% of those given the vaccine developed signs, making the treatment 73% effective.
But when Dubin's group searched for the actual presence of the virus in the women, the results were less heartening. The team discovered that fewer than 50% of the women were actually free of the virus. Still, scientists like Spruance believe this represents progress, since the symptoms of genital herpes are so onerous.
UNANSWERED QUESTIONS. The results raised a number of questions. Why, for example, weren't men protected against the virus? Spruance hypothesizes that the gender gap in the vaccine's efficacy is explained by anatomical differences between the sexes and not by sex differences in the immune system. As proof, he notes that both sexes made equal amounts of antibodies to the virus when vaccinated. Following immunization, woman may be able to build up a supply of immune cells in the vagina to fight off the virus at the point of infection. But that same increase in killer cells doesn't occur in the penis.
Another mystery is why only a subset of women -- those who had never been exposed to any form of herpes -- responded to the vaccine. And then, given that nearly every adult woman has already been exposed to HSV1, what's the practical utility of this particular treatment? The researchers don't yet have an answer to the first question, but they're adamant that despite its limitations, the existing vaccine will be a powerful weapon in the war on herpes.
Dr. Lawrence R. Stanberry, director of the Center for Vaccine Development at the University of Texas in Galveston, says the vaccine could significantly benefit girls under the age of 13 who haven't yet been exposed to herpes. It could also prevent transmission from pregnant mothers to their fetuses, which is usually fatal to the unborn child.
Stanberry points to computer-model studies performed at Oxford University by Dr. Geoffrey Garnett as an indication of the vaccine's potential. Garnett developed powerful software to predict the number of new herpes cases 25 years from now, using the study's figure of 73% of women who were completely symptom-free. His findings suggest that even this level of protection would reduce the incidence of genital herpes by 25% in both men and women. And that, Stanberry says, "is a positive move."
By Ellen Licking at the ICAAC in Toronto Edited by Douglas Harbrecht
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