Recent sexual violence exposure is associated with immune biomarkers of HIV susceptibility in women

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

Association of trauma exposure with proinflammatory activity: a transdiagnostic meta-analysis

Exposure to psychological trauma (for example, childhood/early life adversity, exposure to violence or assault, combat exposure, accidents or natural disasters) is known to increase one's risk of developing certain chronic medical conditions. Clinical and population studies provide evidence of systemic inflammatory activity in trauma survivors with various psychiatric and nonpsychiatric conditions. This transdiagnostic meta-analysis quantitatively integrates the literature on the relationship of inflammatory biomarkers to trauma exposure and related symptomatology. We conducted random effects meta-analyses relating trauma exposure to log-transformed inflammatory biomarker concentrations, using meta-regression models to test the effects of study quality and psychiatric symptomatology on the inflammatory outcomes. Across k=36 independent samples and n=14 991 participants, trauma exposure was positively associated with C-reactive protein (CRP), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α (mean rs =0.2455, 0.3067, 0.2890, and 0.2998, respectively). No significant relationships were noted with fibrinogen, IL-2, IL-4, IL-8, or IL-10. In meta-regression models, the presence of psychiatric symptoms was a significant predictor of increased effect sizes for IL-1β and IL-6 (β=1.0175 and 0.3568, respectively), whereas study quality assessment scores were associated with increased effect sizes for IL-6 (β=0.3812). Positive correlations between inflammation and trauma exposure across a range of sample types and diagnoses were found. Although reviewed studies spanned an array of populations, research on any one specific psychiatric diagnosis was generally limited to one or two studies. The results suggest that chronic inflammation likely represents one potential mechanism underlying risk of health problems in trauma survivors