Aldous Annette M, Joy Christopher, Daniels Jason, Jais Mariel, Simmens Samuel J, Magnus Manya, Roberts Afsoon, Connors Kaleigh, Capozzi Brendan, Mohamed Hani, Juzumaite Monika, Devore Heather, Moriarty Theresa, Hatch Schultz Catherine, Zumer Maria, Simon Gary, Ghosh Mimi
Department of Epidemiology, Milken Institute School of Public Health, The George Washington University, Washington, DC, USA.
Department of Biostatistics and Bioinformatics, Milken Institute School of Public Health, The George Washington University, Washington, DC, USA.
Am J Reprod Immunol. 2021 Sep;86(3):e13432. doi: 10.1111/aji.13432. Epub 2021 May 10.
HIV/AIDS and sexual violence act synergistically and compromise women's health. Yet, immuno-biological mechanisms linking sexual violence and increased HIV susceptibility are poorly understood.
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.
In CVL, Exposed women had significantly reduced chemokines MIP-3α (p < .01), MCP-1 (p < .01), and anti-HIV/wound-healing thrombospondin-1 (p = .03). They also had significantly increased inflammatory cytokine IL-1α (p < 0.01) and were more likely to have detectable wound-healing PDGF (p = .02). In plasma, Exposed women had reduced chemokines MIP-3α (p < .01) and IL-8 (p < .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 < .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.
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.
艾滋病毒/艾滋病与性暴力相互作用，损害了妇女的健康。然而，性暴力与艾滋病毒易感性增加之间的免疫生物学机制却鲜为人知。
我们对未感染艾滋病毒的女性进行了一项横断面试点研究，将过去12周内遭受过强迫阴道插入的13名女性（暴露组）与25名未暴露女性进行比较。对血浆和宫颈阴道灌洗液（CVL）中与艾滋病毒发病机制相关的49种生物标志物进行了酶联免疫吸附测定（ELISA）。采用倾向评分加权法控制年龄、种族、社会经济地位、月经周期和避孕措施的使用，通过线性回归和逻辑回归分析暴露组和未暴露组之间的差异。
在宫颈阴道灌洗液中，暴露组女性的趋化因子MIP-3α（p < 0.01）、MCP-1（p < 0.01）和抗艾滋病毒/伤口愈合的血小板反应蛋白-1（p = 0.03）显著减少。她们的炎症细胞因子IL-1α也显著增加（p < 0.01），并且更有可能检测到伤口愈合的血小板衍生生长因子（p = 0.02）。在血浆中，暴露组女性的趋化因子MIP-3α（p < 0.01）和IL-8（p < 0.01）、抗炎细胞因子TGF-β（p = 0.02）、抗艾滋病毒/抗菌的人β-防御素-2（p = 0.02）以及伤口愈合的基质金属蛋白酶-1（p = 0.02）减少。她们的血小板反应蛋白-1（p < 0.01）和组织蛋白酶B（p = 0.01）也增加。在应用严格的错误发现率调整方法后，宫颈阴道灌洗液中IL-1α（p = 0.05）和MCP-1（p = 0.03）以及血浆中MIP-3α（p = 0.03）的差异仍然显著。
我们报告了遭受性暴力的女性存在全身和黏膜免疫失调。由于这些生物标志物与艾滋病毒发病机制有关，失调可能会增加艾滋病毒易感性。
