NEW YORK (Reuters Health) May 09 - Topical therapy with the investigational immune response modifier resiquimod decreases genital shedding of herpes simplex virus type 2 (HSV-2), researchers report in the May 1st issue of the Journal of Infectious Diseases.
Dr. Karen E. Mark of the University of Washington, Seattle and colleagues note that the agent, an imidazoquinolinamine, stimulates production of cytokines that promote an antigen-specific T helper type 1 cell-mediated immune response. In animal models, they add, induction of such responses modifies experimental HSV infection.
"Resiquimod works differently," from other antiviral agents, Dr. Mark told Reuters Health, "by enhancing the body's own immune system to decrease the number of future herpes outbreaks. Currently available drugs for treating genital herpes act by directly targeting the virus to shorten symptoms of a genital herpes outbreak or to prevent outbreaks while taking pills daily."
To assess the efficacy of resiquimod 0.01% gel for reducing human anogenital HSV-2 mucosal reactivation, the researchers studied 75 subjects with genital HSV-2 who were randomized to apply the agent or the vehicle gel alone to herpes lesions twice weekly for 3 weeks.
Daily anogenital swabbing was used to evaluate shedding over the next 60 days. Recurrences during the subsequent 7 months were treated with the study gel, and during the final 60-day treatment-free period, swabs were again employed to gauge shedding.
The median lesion rates (the proportion of days with lesions) during the initial sampling period were 10% in the resiquimod group and 16% in the vehicle group. Corresponding shedding rates (the proportion of days with detectable HSV DNA) were 10% and 17%.
In the final sampling period, lesion rates were 3% in the resiquimod group and 22% in the vehicle group. Shedding rates were 10% and 26%.
"This suggests," concluded Dr. Mark, that "a reduction in shedding of the herpes virus from the genital tract, and thus likely a reduction in sexual transmission of genital herpes, will be possible with the further development of drugs which work by a similar mechanism as resiquimod. More studies will be needed to confirm these findings."
J Infect Dis 2007;195:1324-1331.
Source:
http://www.medscape.com/viewarticle/556264?src=mp
