Track A Basic Science

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138319/1/jia218438.pd

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

Author summary Schistosomiasis is a parasitic disease that is common in many parts of sub-Saharan Africa most affected by the HIV-1 epidemic. Schistosomiasis causes genital damage when schistosome ova become lodged in the female genital tract, inducing inflammation that may elevate HIV-1 genital viral loads and increase the risk of HIV-1 transmission. Schistosomiasis may also promote viral replication by facilitating cell-to-cell transmission of HIV-1, elevating HIV-1 plasma viral load levels. Using data from 370 individuals residing in Kenya or Uganda who acquired HIV-1 while participating in one of four prospective cohort studies, we tested the hypotheses that schistosomiasis increases plasma and genital viral load levels. We found no evidence that individuals with schistosomiasis had higher set point plasma viral load levels, a measure of viral replication obtained during the set point period 4-24 months after HIV-1 acquisition when viral load levels remain relatively stable. Additionally, we found no evidence that schistosomiasis was associated with higher female set point genital viral loads measured from vaginal or cervical swabs. Unexpectedly, we found that S. mansoni infection was associated with a decline in plasma viral load levels while S. haematobium infection was associated with a decline in cervical viral load levels. Thus, our results do not support the hypotheses that schistosomiasis increases plasma and 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 log(10) copies/ml, 95% CI -0.38 to 0.03); S. mansoni infection was associated with a lower set point (-0.34 log(10) copies/ml, 95% CI -0.58 to -0.09). We found no association between schistosomiasis and cervical (+0.07 log(10) copies/swab, 95% CI -0.20 to 0.34) or vaginal (+0.11 log(10) 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 log(10) copies/swab, 95% CI -1.11 to -0.06).Host-parasite interactio