In recent studies we determined that expression of HSV latency transcripts modulate disease reactivation, but the absolute quantity of latent viral DNA in ganglia is the major determinant of reactivation rates. We are using mice deleted for expression of various cytokines to explore immune regulation of latency and reactivation. Most recently, we have created a mouse transgenic for HSV latency-associated transcripts. A variety of clinical studies are being undertaken that complement these laboratory investigations. Among the accomplishments of such studies was the development of acyclovir for suppression of recurrent genital and oral herpes, demonstration of asymptomatic virus shedding in infected men and women, and completion of the first human trials of recombinant glycoprotein vaccines for genital herpes.
Additional studies examine the ability of antiviral drugs to prevent transmission of genital herpes.
Lekstrom-Himes, J.A., Hohman, P., Warren, T., Wald, A., Nam, J.M., Simonis, T., Corey, L., and Straus, S.E. Association of major histocompatibility complex determinants with development of symptomatic and asymptomatic genital Herpes Simplex Virus Type 2 Infections. Journal of Infectious Diseases. S.E. The quantity of latent viral DNA correlates with the relative rates at which Herpes Simplex Virus Types 1 and 2 cause recurrent genital herpes outbreaks. Journal of Virology. Journal of Virology.