HIV and Herpes: Dangerous Partners

In the past year there has been a lot of eye-opening information emerging on genital herpes that is affecting how we clinically suspect, diagnose, test, and treat the disease in both HIV-negative and HIV-positive adults. We now have Food and Drug Administration'approved blood tests for antibodies to HSV-1 and HSV-2, two of the most common herpes virus types. Surveys show that the prevalence of HSV-2 is almost 1 in 3 in the general U.S. population and as high as 50% to 60% among HIV-positive men and women. Much of the data comes from better methods used to identify the presence of HSV on the skin, even when herpes lesions aren't present. Compared to the old methods of viral culture and identification from swabs from the skin, a new test'PCR (polymerase chain reaction)'is four times more likely to detect the presence of HSV. PCR also distinguishes between HSV-1 and HSV-2, the latter of which causes 98% of genital outbreaks. Through this more sensitive testing, we now know that genital herpes appears in many forms other than the standard painful blistery eruption. And while we used to think that herpes was present on the skin only when such lesions were present'and thus it was the only time that virus could be transmitted to a sex partner'persons infected with HSV-2 have now been shown to have detectable virus on their skin an unnerving 10'12 days each month, even when they are otherwise symptom-free. Up to 70% of HSV transmissions occur during these asymptomatic times. Even worse is the fact that within the first year of acquiring HSV-2, the number of days of viral shedding is even greater, boosting transmission odds even more. The herpes simplex virus lies dormant along a nerve root under the skin. When it activates, the skin or mucous membrane typically blisters and then erodes into an open ulcer. But we now know that at other times there may be microscopic ulcers present, and these account for the asymptomatic viral shedding and the atypical presentations. In these ulcers, big or small, are large numbers of activated CD4 cells. Just like HIV, HSV infects and then reproduces in these cells. Because large numbers of CD4 cells are present in these microscopic lesions, there are often high levels of HIV there as well in people who are HIV-HSV coinfected. HIV viral loads throughout the body also have been shown to rise during herpes outbreaks. Because more HIV is present both on the skin and potentially in sexual fluids, the odds of transmitting the virus to sex partners is boosted. The presence of microscopic or visible herpes lesions on HIV-negative people also makes them much more likely to become infected with HIV'four to five times more likely, according to some studies, because HIV can easily enter through these open sores. Fortunately, we now have data that shows daily HSV suppression with any of the three antiherpes medications'acyclovir, famciclovir, and valacyclovir'can reduce the days of HSV shedding in both HIV-positive and HIV-negative men and women. And although there are no definitive studies yet to prove that such herpes suppression strategies can help lower HIV risks, many clinicians believe that preventing these herpes outbreaks'especially the unnoticed microscopic kind'does reduce the odds of HIV transmissions. As such, I highly recommend that testing for HSV antibodies and the use of herpes suppressive medications, if needed, be a serious topic for discussion between every patient'HIV-positive and HIV-negative'and his or her clinician. Bowers is board-certified in family practice and is a senior partner with Pacific Oaks Medical Group, one of the nation's largest practices devoted to HIV care, located in Beverly Hills. He has served on the boards of AIDS Research Alliance and Lambda Legal. He is on the editorial board of Postgraduate Medicine.