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In the news ... 2007

Two studies highlight the role of herpes
infection in HIV disease

November 28, 2007

Two studies reported in the November 15, 2007 issue of the Journal of Infectious Diseases (JID) highlight the role that herpes infection plays in HIV activation and likely on the risk of transmission.

The first study found that successful suppression of Herpes Simplex Virus (HSV) reduced HIV levels in both plasma and rectal secretions in men. The study was performed in Peru and included 20 men who had never taken anti-HIV drugs, had CD4 counts above 200 and were co-infected with HSV.

At the start of the study, half of the participants were randomly assigned to take either valacyclovir (sold as Valtrex in the US) or placebo for 8 weeks. After two weeks, the groups were switched- with the placebo group taking valacyclovir and the valacyclovir group given a placebo (called a cross-over study design). The study was double blind, meaning neither the participants nor the researchers knew which group the volunteers were in.

Samples of blood plasma and rectal mucosal secretions were taken throughout the study and tested for levels of both HSV and HIV. The researchers found that HIV levels were reduced by around a third in rectal secretions and about half in blood plasma when people were taking valacyclovir. The reductions were greatest in people with higher CD4 counts. This research confirms earlier findings from a study of women in Burkina Faso, which found similar reductions in HIV levels when participants were also given valacyclovir.

Valacyclovir does not have any direct anti-HIV activity. The reductions in HIV levels observed in the study are thought to be an indirect result of reducing HSV activity. Other research has found that HIV levels increase during symptomatic herpes outbreaks. It is possible that by reducing HSV levels, there is also a reduction in localized immune activation, which leads to a reduction in HIV levels.

The second study presented in the same issue of JID found that immune system cells of women with genital ulcerative disease (GUD) usually caused by either HSV or syphilis had higher levels of the co-receptor called CCR5, which HIV can use to gain entry into cells. Levels of another co-receptor, called CXCR4, were not increased. CCR5 is thought to be associated with new HIV infection and early HIV disease, while CXCR4 is thought not to play a significant role in HIV transmission.

The authors of that study speculate that this finding might help explain the higher risk of HIV infection in people with GUD. They believe that immune system cells recruited to the area of an outbreak of either herpes or syphilis are likely to allow very efficient HIV infection due to the high levels of CCR5 they contain.

Taken together, these two studies further reinforce the growing body of evidence of the important role that herpes infections play in both HIV transmission on HIV disease progression. Herpes is among the most common co-infections for people with HIV. These two studies suggest that successful suppression of herpes outbreaks is likely to somewhat slow HIV disease progression and reduce the risk of HIV transmission through sexual contact.

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