Associations between schistosome infection and incident HIV not mediated by STIs or vaginal dysbiosis in a longitudinal cohort of Zambian women Restricted; Files Only
Kaabi, Oumaima (Spring 2022)
Published
Abstract
Introduction. Schistosomiasis affects over 240 million people worldwide. The species S. haematobium causes urogenital schistosomiasis and is most common in Zambia. Female genital schistosomiasis (FGS) is associated with increased risk of HIV, but the mechanism requires further elucidation. FGS is suspected to increase women’s risk for sexually transmitted infections (STIs) and vaginal dysbiosis which are known HIV risk factors. In this analysis we test whether STIs, vaginal dysbiosis, and genital ulcers are mediators for the association between schistosomiasis and HIV risk in women who participated in a longitudinal cohort of heterosexual HIV serodiscordant couples in Zambia.
Methods. Data and samples were collected from a prospective cohort in Lusaka, Zambia from 1994-2009. Baseline demographic variables are presented using descriptive statistics. We use Cox survival models to evaluate whether genital inflammation, STIs (gonorrhea, chlamydia, trichomonas), bacterial vaginosis (BV), candida, and genital ulcers are mediators of the association between schistosomiasis and HIV by evaluating their association with schistosome-specific (SS) antibody status. Data are stratified by HIV status and SS antibody status.
Results. 50% of HIV+ women (n=596) had positive SWAP ELISA results at baseline compared with 55% of HIV- women (n=503). Schistosome infection was not significantly or meaningfully associated STIs, genital inflammation, bacterial vaginosis (BV), candida, or genital ulcers. SS+ women were less likely to be pregnant at baseline and more likely to have a partner who is also SS+. SS+/HIV+ women were more likely to be in HIV Stage III-IV than SS-/HIV+ women. In HIV+ women, SS+ status was associated with lower levels of unprotected sex and fewer incident pregnancies.
Discussion. The data from this cohort does not support the hypothesis that the association between FSG and HIV risk is mediated by STIs. This is one of the first studies to use data from a large, robust, observational cohort to evaluate this hypothesis. Future studies should examine other mechanisms that may explain the relationship between FGS and HIV including genital tract damage facilitating HIV entry or changes in immune markers leading to increased HIV risk. Understanding this pathway will inform more targeted interventions that can control the HIV epidemic in the region.
Table of Contents
Chapter I: Background and Literature Review
Schistosomiasis Epidemiology
Schistosomiasis and HIV
Mechanisms
Praziquantel Treatment
Sociocultural Context and Ethical Considerations
Chapter II: Manuscript
Abstract
Introduction
Methods
Results
Discussion
Chapter III: Public Health Implications and Future Directions
Tables and Figures
References
About this Master's Thesis
| School | |
|---|---|
| Department | |
| Subfield / Discipline | |
| Degree | |
| Submission | |
| Language |
|
| Research Field | |
| Palabra Clave | |
| Committee Chair / Thesis Advisor |
Primary PDF
| Thumbnail | Title | Date Uploaded | Actions |
|---|---|---|---|
|
|
File download under embargo until 23 May 2024 | 2022-04-07 11:43:52 -0400 | File download under embargo until 23 May 2024 |
Supplemental Files
| Thumbnail | Title | Date Uploaded | Actions |
|---|