Infection with schistosome parasitic worms has an important role in HIV transmission, especially for women, and may accelerate HIV disease progression, according to research published in PLOS Neglected Tropical Diseases. Women with schistosomiasis had a three-fold increased risk in becoming infected with HIV, compared to women who did not carry the worms. Moreover, HIV viral load after infection was higher among schistosome-infected individuals, increasing both their potential infectiousness to sex partners and the risk of HIV disease progression.
“Our study suggests that interactions exist between HIV-1 and schistosomiasis that may play a critical role in HIV-1 transmission and disease progression in African countries,” comment the investigators.
Schistosomiasis is a disease caused by a tropical parasitic worm infection. Over 90% of infections occur in Africa. The worms live in small veins in host’s pelvis and gut and daily lay hundreds of eggs that migrate to the urogenital and gastrointestinal mucosa where they cause inflammation and physical breaches in the mucosa.
A team of investigators postulated that pre-existing schistosome infection would increase a patient’s risk of acquiring HIV, with the risk especially high for women. They also hypothesised that individuals with active schistosome infection at the time of HIV acquisition would have impaired immune systems, resulting in higher HIV viral loads.
To test these hypotheses, the researchers designed a nested case-controlled study involving adults living in rural Tanzania. In 2007, 2010 and 2013 participants were tested for HIV.
The investigators identified 73 individuals who became infected with HIV during follow-up. These people were matched with 265 controls who remained HIV negative. Dried blood spots from the cases and controls were tested for the presence of schistosome infection to see if it increased the risk of acquiring HIV.
The investigators also compared the viral loads of HIV seroconverters according to schistosome-infection status.
In women, 44% of those who acquired HIV had schistosome infection at the time of their seroconversion compared to 30% of the HIV-uninfected controls. After taking into account potential confounders, the investigators showed that women with schistosome infection had an almost three-fold increase in the risk of becoming infected with HIV compared to women who remained HIV negative (OR = 2.8; 95% CI, 1.2-6.6, p = 0.019).
Just under a third (29%) of men who seroconverted for HIV had schistosomiasis at the time they became infected with HIV, compared to a schistosomiasis prevalence of 38% among men who remained HIV negative. As such, the schistosome infection did not increase the risk of HIV acquisition for men.
“We found that schistosomiasis increases the odds of HIV-1 acquisition in women but not men,” comment the researchers. “This strong gender effect may be due to differential effects of schistosome eggs in the genital mucosa of women versus men.”
Among people who did become infected with HIV, median viral load was approximately 25,000 copies/ml among those with schistosomiasis compared to 5000 copies/ml among individuals who did not carry the parasitic infection, a significant difference (p = 0.017). Viral load differences by schistosomiasis-infection status were more pronounced in women.
“We found that schistosomiasis at the time of HIV-1 infection led to a 0.7 log10 increase in viral load at the time of HIV-1 seroconversion,” write the authors. “A sustained 0.7 log10 HIV-1 load increase equates with an approximate doubling of infectivity among HIV-1-schistosome co-infected individuals and would be expected to accelerate time to symptomatic AIDS or death by 2-3 years.”
The authors conclude that schistosomiasis increases HIV incidence among women and raises viral load at the time of seroconversion. They note that praziquantel is a cheap and safe treatment for schistosomiasis and call for studies to determine the effectiveness of mass therapy with this drug to decrease HIV transmission and slow HIV disease progression.
Author: Michael Carter