International Programs
- Brazil
- Guatemala
- India
- Mexico
- Mozambique
- United States
Funding Source: National Institute of Allergy & Infectious Diseases (R01-AI-128803-01)
PIs: Jamila K. Stockman, PhD, MPH and Mimi Ghosh, PhD, MS
Although the association between sexual violence and HIV among girls and women is largely attributed to high risk behaviors, underlying biological mechanisms also play a role, but are poorly understood. Sexual violence may contribute to increased susceptibility to HIV infection by disrupting the uterine cervix and the vagina and increasing local inflammation and immune activation. Sexual violence may also disrupt the hypothalamic-pituitary-adrenal (HPA) axis resulting in changes to the innate and adaptive immune system in the female genital tract (FGT) and alterations to the uterine, cervical, and vaginal health. When compared to adult women, adolescent girls may be at heightened biological risk due to cervical ectopy and high baseline inflammation in the female genital tract (FGT), rendering girls more vulnerable to adverse effects of stress. Our preliminary data indicate both recent and chronic cases of sexual violence cause dysregulation of critical FGT immune mediators that have the potential to affect HIV susceptibility.
Establishing a better understanding of the correlation between immunity in the FGT and the dysregulated HPA axis, as well as the differences between adolescent girls and adult women is critical for the development of strategies to counter the adverse effects of sexual trauma resulting from mucosal injury in efforts to reduce the risk of HIV acquisition. This study seeks to expand our knowledge base on the potential biological differences between adolescent girls and adult women in terms of susceptibility to HIV in the context of sexual trauma and has implications for hypothesis-driven longitudinal research and development of safe and effective biomedical prevention strategies for populations at heightened risk of HIV infection.