Presented by A Wald. University of Washington, Seattle, WA, USA.

The epidemic of HSV-2 is driven by the ability of the virus to be transmitted during periods of asymptomatic or subclinical shedding. Most sexual and perinatal transmission of HSV occurs during asymptomatic viral reactivation. Our ability to measure the frequency of reactivation has been advanced with the development of HSV DNA PCR which is up to 4 times more sensitive than viral culture in detecting the virus on mucosal surfaces. Among HSV-2 seropositive persons, genital HSV shedding occurs on a median of 19% of days (range 0–96) and the spectrum of symptoms is also wide. This large variability in HSV-2 genital shedding rate as well as in the symptoms is poorly understood and appears mostly determined by host factors. Viral type – HSV-2 vs. HSV-1 – and time since HSV-2 acquisition are the only known determinants of HSV reactivation. These factors, however, explain only a small portion of the observed variability. HIV infection increases the rate of genital HSV shedding both in frequency and in quantity. Highly active antiretroviral therapy ameliorates clinical HSV disease but has little effect on viral reactivation rates. Recent PCR-based studies of oral HSV reactivation show that HSV-2 shedding in the mouth is not infrequent among HIV infected patients.

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