This project is investigating HIV and Hepatitis C risk among injection drug users in central rural Puerto Rico and ultimately, aims to use this research to reduce the spread of HIV and Hepatitis C in Puerto Rico by identifying effective prevention strategies.
Between 2014 and 2019, we will interview more than 600 people who inject drugs and ask them about their risk behaviors, injection risk partners, and about their lives in rural Puerto Rico. Each participant will also complete a rapid HIV and Hepatitis C test. The analytical portion of the project involves simulating risk social networks on a regional scale, and testing the simulation effects of a range of interventions.
The Opioid Agonist Treatment (OAT) Project:
The OAT research project aims to understand the individual and social barriers to accessing OAT among persons who inject drugs in rural Puerto Rico. Understanding what prevents persons who inject drugs from entering and continuing OAT treatment might contribute to a higher treatment coverage which has been severely restricted in the aftermath of hurricane Maria.
PR Biome Project:
The PR BIOME project is funded by the National Institutes of Health and is overseen by researchers and staff from the University of Nebraska in collaboration with the University of Puerto Rico and the Central Caribbean University. In the field, the VIDA, ACCIÓN, SALUD (VAS or Life, Action, Health in English) team will carry out the project in Puerto Rico. In the last five years, the VAS team has carried out several projects in Puerto Rico. Previous projects and funding allowed us to learn more about people using injectable drugs and the risk of HIV and HCV.
Our most recent project, Biomarkers for Dysbiosis-Related HIV-Associated Cognitive Disorders among Persons Who Inject Drugs in Puerto Rico, now aims to understand the effects of HIV infection and the use of injectable drugs on the microbiome, with the goal of discovering biomarkers for the progression of neurological diseases among PWID that are related to chronic inflammation and coupled inflammation of dysbiosis. A prospective and multi-cohort longitudinal study will allow repeated measurements of the study population and compare them with similar measures from control groups of non-HIV-infected and non-HIV-infected users from the same site. This longitudinal evaluation will allow our team to test the hypothesis that HIV-1 infection in PWID intensifies dysbiosis and inflammation, which in turn exacerbates HIV replication, HAND and HIV treatment failures. We hope that this hypothesis, if true, will have important implications for the emerging drug epidemic in the rest of the United States.