Genital herpes (caused by herpes simplex virus type 1 and, more commonly, type 2) is one of the most common sexually transmitted diseases in the world. It is found in one in five Americans and in more than 80% of people with HIV, where the two viruses significantly affect each other.
People with HSV-2 are two to three times more likely to pick up HIV. When HSV-2 erupts, HIV viral loads can rise and genital ulcers are teeming with HIV and T cells. Suppression of HSV-2 reduces the amount of HIV in blood and genital secretions.
Now, two studies have looked at the effects of HSV suppression on HIV transmission. The first study involved about 3,200 volunteers infected with HSV-2 from the United States, South America, and Africa and included heterosexual women and men who have sex with men. Participants got either 400 milligrams of acyclovir twice a day or placebo. Everyone received extensive safer-sex counseling and condoms. But at the end of the study 3.9% on acyclovir had picked up HIV compared to 3.3% on placebo, even though the group on acyclovir had a 35% reduction in genital ulcers.
The second study involved 3,400 African couples in which one partner had both HIV and HSV-2 and the other had neither. Half of the partners infected with both viruses received 400 milligrams of acyclovir twice a day, and half received placebo. Again, there was no difference in HIV transmission: 41 infections in the acyclovir arm and 43 infections in the placebo arm. Genital ulcers decreased 73% and the HIV viral load decreased by 40% in the acyclovir group. Interestingly, the rate of HIV disease progression slowed by 17% in the treated group.
A possible explanation for these results can be found in a paper published in Nature Medicine in August. In this study multiple biopsies were taken from HVS-2-positive/HIV-negative women and men at various time points and locations including active genital ulcers, healed ulcer sites at various intervals over 20 weeks, and normal genital skin that had never had herpes eruptions.
They made four interesting discoveries:
(1) CD4 cells were found at healed ulcer sites in concentrations two to 37 times greater than unaffected skin, and treatment with acyclovir did not reduce these high concentrations.
(2) CD4 cells in the ulcer sites were twice as likely to have the CCR5 attachment molecule that HIV uses, compared to normal skin.
(3) Ulcer sites had significantly higher numbers of dendritic cells of the type that transport HIV to the T cells.
(4) HIV replicates three to five times faster in tissue from the ulcer sites compared to normal skin.
In a nutshell, these studies show that what we really need is a herpes vaccine. But in the meantime, we still need to treat HSV-2 to reduce its transmission and to take its pressure off HIV replication.
Bowers is an HIV specialist and is board-certified in family medicine. He is in private practice in New York City. Learn more about Bowers at https://www.danbowersmd.com
