Jul 02, 2010
Genital Herpes (HSV2) and HIV disease: Why does it matter?
There is good evidence from population studies of people infected with both HIV1 and also HSV2 that infection with Herpes Simplex 2 virus will both increase the amount of HIV1 which is shed in gental secretions and also it increases the rate at which HIV 1 is transmitted.
Treatment designed to suppress Herpes simplex 2 (HSV2) is established to reduce the amount of HIV1 RNA in blood and also genital secretions such as semen and vaginal secretions.
The impact of co-infection (having infection with HIV and HSV2) of HIV1 and HSV2 is very significant indeed with HSV2 and HIV1 co-infected individuals having very much more HIV1 RNA (ie the infectiouness of the individual is increased) in their genital secretions and also in their blood. This obviously means that their potential for spreading HIV either through asymptomatic HSV shedding or symptomatic HSV2 lesions is greatly increased. In addition, treatment for the HSV2 part of the co-infection has no effect on the HIV1 directly but does reduce the HIV1 viral load.
HIV viral load increases are associated with an accelerated course towards the development of AIDS defining diagnoses (AIDS is not the same as being HIV positive). The way anti HSV2 medications reduce HIV1 viral load is thought to be through partly interupting the “HIV inducing effect” of HSV2.
Unfortunately, we also know that people with HSV2 genital lesions are much more likely to acquire HIV1 from an HIV infected individual – by a factor of up to six times more likely.
Up to 60% of people living in the “West” with HIV have Herpes Simplex 2 (HSV2) infections whereas in Sub-Saharan Africa the figure is thought to be up to 90%.
A study by Nagot and others published in the NEJM (Nagot N, Ouedraogo A, Foulongne V, et al. Reduction of HIV-1 RNA levels with therapy to suppress herpes simplex virus. N Engl J Med 2007;356:790-9) looked at HIV1 and HSV2 co-infected populations in Sub-Saharan Africa and treated trial subjects with valaciclovir, an anti-HSV2 drug.
HIV1 is shed from HSV2 lesions and most of the shedding (85%) occurs without the actual physical appearance of HSV2 genital ulcers.
The effects were to markedly reduce the re-occurence of HSV2 lesions, and to markedly reduce the amount of HIV1 in both blood and also genital secretions.
The significance of this is that reducing the HIV1 viral load in the genital tract by treating the additional HSV2 infection may reduce the transmissibility of HIV1 infections (and probably HIV2 although this was not within the studied populations).
A further possible scenario is that people with HSV2 but not HIV will be at theoretically reduced risk of HIV acquisition if they suppress the appearance of HSV2 lesions by long term suppressive treatments such as aciclovir or valaciclovir. Aciclovir has the great advantage of being very cheap and very well tolerated.