Genital herpes associated with higher genital and plasma HIV viral load in women

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Women with genital ulcers as a result of the herpes simplex virus have more HIV in both their blood and their cervicovaginal fluid, according to French researchers writing in the July 31st edition of AIDS.

Being infected with herpes simplex virus (HSV) type 2 increases the risk of HIV infection by as much as eightfold but exactly how much the presence of acute HSV-2 symptoms, particularly genital ulcers, increases the risk of transmissibility is less clear.

One study in HIV-serodiscordant couples in Uganda reported that if the HIV-infected partner also had genital ulcers then the risk of HIV transmission was increased fourfold. But it was not clear in that study whether the ulcers were caused by HSV-2, although the virus is the most common cause of genital ulcer diseases.


herpes simplex virus (HSV)

A viral infection which may cause sores around the mouth or genitals.


Viral shedding refers to the expulsion and release of virus progeny (offspring such as competent particles, virions, etc.) following replication. In HIV this process occurs in the semen, the vaginal secretions and other bodily fluids, making those fluids more infectious.

genital ulcer disease

Any of several diseases that are characterised by genital sores, blisters or lesions. Genital ulcer diseases (including genital herpes, syphilis and chancroid) are usually sexually transmitted.


The fluid portion of the blood.


A break in the skin or mucous membrane which involves the loss of the surface tissue.


The authors of this new study have analysed the effect of having genital HSV ulceration on HIV levels in the plasma and cervicovaginal fluid of 441 women in Ghana and the Central African Republic. The women are taking part in a study to find out how giving treatment for the HSV infection affects HIV and HSV shedding and the analysis was carried out before treatment started.

Of the 441 women studied, 79% were HSV-2 infected, 46.6% were HIV-positive and 50% had a HSV-2-related ulcer at the time of study. Ulcers were more likely among younger women, probably reflecting a more recent infection, and among HIV-infected women, especially those who showed signs of immunosuppression.

Among the 180 women infected with both HIV and HSV-2, cervicovaginal HIV was detected in 68% of those who had a HSV-2 ulcer, compared to 42% of those who did not (p = 0.004). On average, women with genital HSV-2 ulcers had higher average cervicovaginal HIV RNA loads (3.14 log10 copies/ml versus 2.10 log10 copies/ml; p = 0.003).

They also had higher average plasma HIV loads (5.10 versus 4.65 log10 copies/ml; p = 0.07, although this difference was not statistically significant) and lower CD4 cell counts (198 versus 409 cells/mm3, p = 0.03). A tenfold increase in cervicovaginal HSV-2 DNA was associated with a 1.7-fold increase in plasma HIV (p = 0.003).

The authors say this is the largest recorded series of patients with genital ulcers in west and central Africa and shows that clinical episodes of genital herpes are associated with increased cervicovaginal and plasma HIV loads.

The results emphasise the interaction between the two viruses and highlight the role of HSV-2 as an important co-factor for HIV transmission, they conclude.

However, several recent studies which have investigated the HIV prevention benefits of HSV-2 suppressive therapy have shown varying degrees of risk reduction when either valaciclovir or aciclovir were used. Valaciclovir reduced genital HIV shedding in HIV-positive women in a randomised study carried out in Burkina Faso, but a Thai study using aciclovir resulted in more modest reductions in genital HIV shedding, while a South African study showed no significant reduction in HIV shedding whatsoever in women who received aciclovir.


Le Goff J et al. Cervicovaginal HIV-1 and herpes simplex virus type 2 shedding during genital ulcer diseases episodes. AIDS 21: 1569-1578, 2007