Schistosomiasis treatment improves CD4 count, viral load in HIV-positives

Treatment of the parasitic infection schistosomiasis (also known as bilharzia) results in a stabilisation in HIV viral load and an improvement in CD4 cell count in HIV-positive people, Danish and Zimbabwean researchers report in the December 1^st edition of the Journal of Infectious Diseases.

Schistosomiasis is a widespread parasitic infection in southern Africa. It is a debilitating parasitic disease caused by five different kinds of flatworm or blood fluke (helminth). 500 to 600 million people are at risk worldwide, in 74 countries, of whom 20 million are severely ill, another 120 million have some symptoms and another 60 million or more are infected. Its economic impact is second only to malaria, in reducing productivity at work and in limiting children’s ability to learn.

It is common in large parts of Africa with two main kinds – S. mansoni (whose eggs are shed into faeces) and S. haematobium (whose eggs are shed into urine). Eggs pass into water where they rest on water plants, until eaten by snails where they grow into larvae that are then shed into fresh water. These larvae then pass into the bodies of people who enter the water.

The schistosomiasis and HIV cohort was established in Zimbabwe to look at the interaction between schistosomiasis and HIV, following the observation that generalised immune activation caused by schistosomiasis might increase the rate of HIV disease progression.

As part of the cohort’s research a randomised study was carried out to test the effects of schistosomiasis treatment in HIV-positive people. The study randomised 287 people with and without HIV infection who were infected with schistosomiasis to receive immediate treatment with praziquantel or treatment deferred for three months.

Two hundred and twenty-eight participants were available for follow-up, of whom 130 were HIV-positive. Comparison between HIV-positive participants who received immediate treatment and those who received deferred treatment showed a difference of –0.21 log₁₀ copies/ml after three months, favouring the immediate treatment group (p=0.03). In the deferred treatment group viral load continued to rise whilst it stabilised in the immediate treatment group.

CD4 counts rose in all patients who received treatment irrespective of HIV status, suggesting that schistosomiasis is a widespread cause of immune suppression in Africa, and further highlighting the need for cohort studies in sub-Saharan Africa outside South Africa that can quantify the relationship between viral load, CD4 count and disease progression, in order to determine whether there are regional differences in the predictive value of internationally recognised thresholds such as a CD4 cell count of 200 cells/mm³.

Using data from a European cohort, the authors estimate that a decrease in viral load of –0.21 log₁₀ copies/ml would be associated with a reduction in mortality of between 1.9 and 7-fold. However they caution that the 95% confidence interval for the viral load change was between –0.39 log and 0.02log₁₀ copies/ml, and that another study has shown any suppressive effect of schistosomiasis treatment on HIV viral load disappearing after six months. They conclude that while their study supports the view that schistosomiasis increases HIV viral load, further operational research is needed to determine whether schistosomiasis interventions should be incorporated into the current initiatives for providing antiretroviral treatment in areas where both infections are endemic.