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NEW YORK (Reuters Health) - People with genital herpes are often prescribed a drug, such as valacyclovir or acyclovir, to take on an ongoing basis to reduce recurrences. However, while both of these antivirals are very effective at suppressing herpes virus shedding, neither completely blocks viral replication, according to new research findings.
In a study, 69 men and women with genital herpes were each treated for 7-week periods with valacyclovir, acyclovir, and an inactive placebo pill, with the courses given in random order.
The participants provided daily genital swabs, which the researchers used to check for the presence of herpes virus by culturing the samples as well as by examining them with a sensitive DNA method called PCR.
According to a report in The Journal of Infectious Diseases, the virus was detected at least once by PCR in 98 percent of the participants, and at least once by culture in 90 percent.
Dr. Rachna Gupta of the University of Washington in Seattle, and colleagues report that shedding of herpes virus occurred on 15 to 40 percent of days, depending on which detection method was used.
Of note, however, many of these episodes of viral reactivation did not cause clinical problems for the patient -- between one-third and one-half of the time when virus could be detected on placebo treatment, there were no actual lesions.
Furthermore, "While subjects were receiving therapy with acyclovir or valacyclovir, most of the (virus)-positive days were subclinical in nature."
Also, both valacyclovir and acyclovir were "highly effective" at reducing the frequency and quantity of shedding, the researchers found.
They did note that the effect of the medications on viral shedding "has a time lag," with a 5-day period before viral suppression is achieved. When treatment stops, "the suppression effect lingers and returns to pretreatment levels in 5 days."
"Current antivirals do not achieve an absolute cessation of shedding, but the effect on ... shedding is sustained beyond the half-life of the drug," the team concludes.
SOURCE: Journal of Infectious Diseases, October 15, 2004.
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Page last updated: 25 October 2004 |