Problem: HIV/AIDS and sexual violence act synergistically and compromise women\u27s health. Yet, immuno-biological mechanisms linking sexual violence and increased HIV susceptibility are poorly understood. Methods: We conducted a cross-sectional pilot study of HIV-uninfected women, comparing 13 women exposed to forced vaginal penetration within the past 12 weeks (Exposed) with 25 Non-Exposed women. ELISA assays were conducted for 49 biomarkers associated with HIV pathogenesis in plasma and cervicovaginal lavage (CVL). Differences between Exposed and Non-Exposed were analyzed by linear and logistic regression, using propensity score weighting to control for age, race, socioeconomic status, menstrual cycle, and contraceptive use. Results: In CVL, Exposed women had significantly reduced chemokines MIP-3α (p \u3c.01), MCP-1 (p \u3c.01), and anti-HIV/wound-healing thrombospondin-1 (p =.03). They also had significantly increased inflammatory cytokine IL-1α (p \u3c 0.01) and were more likely to have detectable wound-healing PDGF (p =.02). In plasma, Exposed women had reduced chemokines MIP-3α (p \u3c.01) and IL-8 (p \u3c.01), anti-inflammatory cytokine TGF-β (p =.02), anti-HIV/antimicrobial HBD–2 (p =.02), and wound-healing MMP-1 (p = 0.02). They also had increased thrombospondin-1 (p \u3c.01) and Cathepsin B (p =.01). After applying the stringent method of false discovery rate adjustment, differences for IL-1α (p =.05) and MCP-1 (p =.03) in CVL and MIP-3α (p =.03) in plasma remained significant. Conclusions: We report systemic and mucosal immune dysregulation in women exposed to sexual violence. As these biomarkers have been associated with HIV pathogenesis, dysregulation may increase HIV susceptibility