The human herpesvirus HSV-2 increases likelihood of HIV acquisition, but surprisingly, antiviral drugs against HSV-2 have no effect on the risk of acquiring HIV. Now, a study from VIDI scientists, including staff scientist Dr. Jia Zhu and member Dr. Larry Corey, shows a potential mechanism for the interaction between HSV and HIV. The scientists took biopsies of genital skin during and after herpes outbreaks, and used immunofluorescence to assay the types of cells in that skin. They found a large number of CD4+ T cells, the cells that HIV targets for infection, in the skin from healed lesions months after the lesions disappeared, even if the subjects were taking antiviral drugs. These T cells expressed increased levels of the HIV receptor protein CCR5, which provides a gateway for HIV to enter the cells. In these biopsies, the group also found increased numbers of dendritic cells, which ferry virus particles to T cells. The persistence of both these types of immune cells and their interactions with each other long after herpes lesions healed indicate that an HSV-2 vaccine may be a better strategy than herpes antiviral drugs to reduce HIV acquisition.
Persistence of HIV-1 receptor-positive cells after HSV-2 reactivation is a potential mechanism for increased HIV-1 acquisition. Zhu J, Hladik F, Woodward A, Klock A, Peng T, Johnston C, Remington M, Magaret A, Koelle DM, Wald A, Corey L. Nat Med. 2009 Aug;15(8):886-92