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PLoS Negl Trop Dis. 2019 Nov 20;13(11):e0007886. doi: 10.1371/journal.pntd.0007886. eCollection 2019 Nov.

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

Author information

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.

PMID:
31747411
DOI:
10.1371/journal.pntd.0007886
Free PMC Article

Conflict of interest statement

I have read the journal’s policy and the authors of this manuscript have the following competing interests: RSM has received funding for research, paid to the University of Washington, from Hologic Corporation. All other authors have declared that no competing interests exist.

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