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51 Profound racial and ethnic disparities exist in the prevalence and persistence of sexually transmitted infections, that can impact not only a woman’s life-time wellness but also her offspring’s prospects for a healthy and productive life. Ascendance of specific vaginal pathobionts to the placenta has been associated with newborn inflammation and changes in the placental epigenome creating a basis for further disparities in intellectual and physical performance later in life. In vitro modeling and clinical studies suggest that the mucosal homeostasis is orchestrated by the resident microbiota and complex host-microbe multi-taxa interactions including protozoa, bacteria, and viruses. We have demonstrated a human in vitro model and in women the role of protozoan-viral-bacterial symbiosis and parasite-viral-bacterial coinfections in altering key mediators of innate immunity, including cytokines, chemokines, and galectins. Deciphering the microbiome of the sexually transmitted parasite Trichomonas vaginalis illustrated howmulti-taxa interaction can affect both the parasite fitness and the vaginal Immunobiome equilibrium and it has contributed to the birth of the Parasite Microbiome Project. The microbiomes of other parasites have been implicated in cancer and more broadly in human disease but have been less studied in modeling reproductive outcomes. We have recently provided clinical evidence that pre-existing aberrant immunity can predispose to vaginal dysbiosis and sexually transmitted infections. Moreover, specific combined patterns of cervical and systemic immunity precede and predict onset of viral sexually transmitted disease including HIV-1 and HSV-2. These findings emphasize the importance of understanding and learning to control modifiable factors and pathways preconditioning the mucosal immune barrier that make it vulnerable to vaginal microbiome dysregulation and persistent infections. Psychological stress, anxiety and depression are interlinked with microbiome changes and intrauterine epigenetic reprograming. Socioeconomic stressors and related exposures, behaviors and malnutrition may contribute to reproductive and mucosal health disparities throughmicrobiome-conditioned pathways sharedwith stress, anxiety and depression. S09.3 Understanding the intersection of human sexual contexts, the rectal mucosal immune environment, and HIV transmission Colleen F Kelley Emory University, Atlanta, GA, USA From 2013–2017 in the United States, 72% of new HIV infections occurred among men who have sex with men (MSM), with approximately 70% attributed to rectal mucosal exposure during receptive anal intercourse (AI). HIV transmission probability per exposure event is 18-fold and 50-fold higher for rectal compared to vaginal or penile exposure respectively. There are many potential contributors to this higher transmission risk for rectal exposures. The rectalmucosa is comprised of single-layer columnar epitheliumwhich may be more susceptible to mechanical microtrauma during intercourse than the stratified squamous epithelium that lines most of the penis and vagina. The gut, particularly the distal rectum where HIV transmission is most likely to occur during AI, also contains most of the body’s lymphocytes, many of which are primary HIV target cells. Understanding rectal mucosal HIV transmission biology is essential for designing biomedical prevention interventions, including an effective vaccine, however, the rectal mucosa has been understudied to date. Our group conducts research to understand how real-life, human sexual contexts alter the rectal mucosal immune environment. We are committed to equitable engagement in research for marginalized and underserved populations including MSM and transgender people. Our laboratory uses a variety of immunologic techniques including flow cytometry, transcriptome sequencing, microbiome sequencing, and HIV rectal explant challenges to characterize the rectal mucosal immuneenvironment among relevant populations.Our group is exploring the effects of condomless receptive anal intercourse, chronologic age, asymptomatic sexually transmitted infections, and gender affirming hormone therapy on the rectal mucosal immune environment. This research will contribute to the improved design of biomedical HIV and STI prevention interventions specifically for populations most in need. S09.4 (Oral Abstract Presentation) HIV-associated genital immune biomarkers in the female sex worker population Eleanor Capozzi1, JasonDaniels1, HaniMohamed1, Fernando Cabezas Mejia1, Jennifer Bouey2, David Sternberg3, Mimi Ghosh1 1The George Washington University, Washington DC, DC, USA; 2Georgetown University, Washington DC, DC, USA; 3HIPS, Washington DC, DC, USA Problem: Women are at a higher risk of HIV acquisition; specifically female sex workers (FSW) face a disproportionately high burden of HIV infection. While there is extensive research of the female urogenital tract, less is known regarding how sex work alters genital immune biomarkers. In addition, determining and developing feasible methodology for collecting biological materials from FSWs in the USA remains unexplored. Our objective in this present study was to characterize the genital immune environment, specifically of HIV associated biomarkers in a FSW population compared to non-FSW control women. Methods: We conducted a pilot study consisting of ten FSWs (5 premenopausal and 5 postmenopausal) from the Washington DC area who participated in a survey and provided vaginal swab for testing of a panel of genital immune biomarkers associated with HIV acquisition. Control groups consisted of healthy age matched volunteers who also provided vaginal swabs. Immune biomarkers were assessed by ELISA, and included the following cytokines, chemokines, growth factors and anti-HIV antimicrobials: Interleukin 1-alpha (IL-1α), Interleukin 1-beta (IL-1β), Interleukin-6 (IL-6), TumorNecrosis Factor-alpha (TNFα), Platelet-Derived Growth Factor (PDGF), Interleukin-8 (IL-8), Interferon Gamma-Induced Protein (IP-10), Macrophage Inflammatory Protein-3, 1-alpha, and 1-beta (MIP3α, MIP1α, MIP1β), Regulated Upon Activation, Normal T cell Expressed, and Secreted (RANTES),