For women with Genital herpes, taking oral contraceptives can double the likelihood of actively shedding the virus and so passing on the infection, a new study shows.

The risk is also roughly doubled when women have bacterial vaginosis - vaginal infection characterized by heavy discharge - or when the vagina is colonized by group B strep.

“Even if they are modest associations, they are important because of the widespread use of contraceptives and also because bacterial vaginosis and group B strep are very common vaginal conditions,” said Dr. Thomas L. Cherpes of Magee-Womens Research Institute at the University of Pittsburgh, the study’s lead author.

The study is the largest to date to look at factors involved in shedding of genital herpes virus, HSV-2, in women free of HIV infection. If the findings are confirmed, Cherpes added, “treatment of STDs and other vaginal coinfections may represent a method of decreasing transmission of HSV-2.”

Cherpes said he and his colleagues had originally theorized that bacterial vaginosis would increase HSV-2 shedding. “We were quite surprised to find the association between group B strep colonization and HSV-2 shedding,” he said.

That’s because group B strep vaginal infection is often considered a mild condition that does not cause ill effects in women who are not pregnant, he explained.

In the current study, published in the medical journal Clinical Infectious Diseases, the researchers followed 330 women with HSV-2 for a year, taking vaginal swabs and smears every four months.

Bacterial vaginosis increased the likelihood of viral shedding 2.3 times, while women with group B strep colonization were 2.2 times likelier to shed HSV-2. Women on oral contraceptives had 1.8 times higher odds of shedding the virus.

Just why viral shedding is increased in these circumstances is unclear, Cherpes said, and investigating them could provide important clues to managing herpes infection. “If we understand why these conditions are permissive toward genital shedding of HSV-2 we can understand better what causes the virus to go from a state of latency to reactivation.”

SOURCE: Clinical Infectious Diseases, May 15, 2005.