Aaron F Bochner1,2, W Evan Secor3, Jared M Baeten1,2,4, Govert J van Dam5, Adam A Szpiro6, Sammy M Njenga7, Paul L A M Corstjens8, Romel D Mackelprang2, Nelly R Mugo7, Julie Overbaugh9, Connie Celum1,2,4, Andrew Mujugira10, R Scott McClelland1,2,4, Ruanne V Barnabas1,2,4. 1. Department of Epidemiology, University of Washington, Seattle, Washington, United States of America. 2. Department of Global Health, University of Washington, Seattle, Washington, United States of America. 3. Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America. 4. School of Medicine, University of Washington, Seattle, Washington, United States of America. 5. Department of Parasitology, Leiden University Medical Center, Leiden, the Netherlands. 6. Department of Biostatistics, University of Washington, Seattle, Washington, United States of America. 7. Kenya Medical Research Institute, Nairobi, Kenya. 8. Department of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands. 9. Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America. 10. Infectious Diseases Institute, College of Health Sciences, Makerere University, Kampala, Uganda.
Abstract
BACKGROUND: 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. METHODS/PRINCIPAL FINDINGS: 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). CONCLUSIONS/SIGNIFICANCE: These results do not support the hypotheses that schistosome coinfection increases plasma or genital HIV-1 viral loads.
BACKGROUND: 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. METHODS/PRINCIPAL FINDINGS: 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). CONCLUSIONS/SIGNIFICANCE: These results do not support the hypotheses that schistosome coinfection increases plasma or genital HIV-1 viral loads.