Schistosomiasis was not associated with higher HIV-1 plasma or genital set point viral loads among HIV seroconverters from four cohort studies

by Aaron F. Bochner, W. Evan Secor, Jared M. Baeten, Govert J. van Dam, Adam A. Szpiro, Sammy M. Njenga, Paul L. A. M. Corstjens, Romel D. Mackelprang, Nelly R. Mugo, Julie Overbaugh, Connie Celum, Andrew Mujugira, R. Scott McClelland, Ruanne V. Barnabas

Many regions of sub-Saharan Africa experience a high prevalence of both schistosomiasis and HIV-1, leading to frequent coinfection. Higher plasma HIV-1 viral loads are associated with faster disease progression and genital HIV-1 loads are a primary determinant of HIV-1 transmission risk. We hypothesized that schistosome infection would be associated with higher HIV-1 viral loads in plasma and genital samples.

We utilized data from individuals who HIV-1 seroconverted while enrolled in one of four prospective cohort studies. Plasma and genital viral loads collected 4–24 months after the estimated date of HIV-1 acquisition, but prior to antiretroviral therapy initiation, were included. Detection of circulating anodic antigen in archived blood samples, collected prior to HIV-1 seroconversion, identified participants with active schistosomiasis; immunoblots determined the schistosome species causing infection. Our analysis included 370 HIV-1 seroconverters with plasma viral load results, of whom 82 (22%) had schistosomiasis. We did not find a statistically significant association between schistosomiasis and higher HIV-1 set point plasma viral loads (-0.17 log₁₀ copies/ml, 95% CI -0.38 to 0.03); S. mansoni infection was associated with a lower set point (-0.34 log₁₀ copies/ml, 95% CI -0.58 to -0.09). We found no association between schistosomiasis and cervical (+0.07 log₁₀ copies/swab, 95% CI -0.20 to 0.34) or vaginal (+0.11 log₁₀ copies/swab, 95% CI -0.17 to 0.39) set point viral loads; S. haematobium infection was associated with lower cervical viral loads (-0.59 log₁₀ copies/swab, 95% CI -1.11 to -0.06).

These results do not support the hypotheses that schistosome coinfection increases plasma or genital HIV-1 viral loads.