Oral contraceptives increase herpes shedding
Consuming oral contraceptives can double the risk of active shedding of the herpes virus in women suffering from genital herpes, hence passing on the infection.
Consuming oral contraceptives can double the risk of active shedding of the herpes virus in women suffering from genital herpes, hence passing on the infection.
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.
Researchers from the Magee-Womens Research Institute at the University of Pittsburgh found that 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.
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, treatment of STDs and other vaginal coinfections may represent a method of decreasing transmission of HSV-2.
The researchers had originally theorized that bacterial vaginosis would increase HSV-2 shedding. They were quite surprised to find the association between group B strep colonization and HSV-2 shedding. Group B strep vaginal infection is often considered a mild condition that does not cause ill effects in women who are not pregnant.
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, investigating them could provide important clues to managing herpes infection. If it is known that why these conditions are permissive toward genital shedding of HSV-2 one can understand better what causes the virus to go from a state of latency to reactivation.
Clinical Infectious Diseases,
May 2005
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