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New research helps explain why even an apparently healed Herpes (HSV-2) sore increases the risk of HIV infection. In a study funded by the National Institutes of Health, scientists have discovered that an immune-cell environment conducive to HIV infection that persists at the location of HSV-2 genital skin lesions long after they have been treated, have healed, and the skin appears normal.

"The findings of this study mark an important step toward understanding why HSV-2 infection increases the risk of acquiring HIV and why acyclovir treatment does not reduce that risk," says NIAID Director Anthony S. Fauci, M.D. "Understanding that even treated HSV-2 infections provide a cellular environment conducive to HIV infection suggests new directions for HIV prevention research, including more powerful anti-HSV therapies and ideally an HSV-2 vaccine," he said.

Herpes simplex 2 (HSV-2), one of the most common sexually transmitted infections, increases the risk of HIV infection by a a factor of 2 to 3.  It had been hypothesized that breaks in the skin caused by HSV-2 were the reason; however, recent trials demonstrated that treatment with anti-herpes drugs, such as acylovir, did not reduce the risk as expected. The new research involved taking multiple skin biopsies from herpes patients at different times during disease outbreaks and healing. Microscopic evaluation of the biopsies showed that CD4+ T cells, the cells that HIV primarily infects, stay at the site of the herpes infection at concentrations between 2 and 37 times greater than that of unaffected tissue.

Using biopsies from two study participants, the scientists found laboratory evidence that HIV replicates three to five times as quickly in cultured tissue from the sites of healed HSV-2 lesions than in cultured tissue from control sites.

These findings help explain why people infected with HSV-2 are at greater risk of acquiring HIV than people who are not infected with HSV-2, even after successful acyclovir treatment of genital lesions.

"HSV-2 infection provides a wide surface area and long duration of time for allowing HIV access to more target cells, providing a greater chance for the initial 'spark' of infection," the authors write.

Journal references:

1. J Zhu et al. Persistence of HIV-1 receptor-positive cells after HSV-2 reactivation is a potential mechanism for increased HIV-1 acquisition. Nature Medicine, DOI:10.1038/nm2006 (2009)
2. Celum et al. Effect of aciclovir on HIV-1 acquisition in herpes simplex virus 2 seropositive women and men who have sex with men: a randomised, double-blind, placebo-controlled trial. The Lancet, 2008; 371 (9630): 2109 DOI: 10.1016/S0140-6736(08)60920-4

[via Science Daily]