This study evaluated the relationship between illicit drug use and HIV-1 disease severity in HIV-1–infected patients enrolled in the DREXELMED HIV/AIDS Genetic Analysis Cohort. Because cocaine is known to have immunomodulatory effects, the cytokine profiles of preferential nonusers, cocaine users, and multidrug users were analyzed to understand the effects of cocaine on cytokine modulation and HIV-1 disease severity.
Patients within the cohort were assessed approximately every 6 months for HIV-1 clinical markers and for history of illicit drug, alcohol, and tobacco use. The Luminex human cytokine 30-plex panel was used for cytokine quantitation. Analysis was performed using a newly developed biostatistical model.
Substance abuse was common within the cohort. Using the drug screens at the time of each visit, the subjects in the cohort were categorized as preferential nonusers, cocaine users, or multidrug users. The overall health of the nonuser population was better than that of the cocaine users, with peak and current viral loads in nonusers substantially lower than those in cocaine and multidrug users. Among the 30 cytokines investigated, differential levels were established within the 3 populations. The T-helper 2 cytokines, interleukin-4 and -10, known to play a critical role during HIV-1 infection, were positively associated with increasing cocaine use. Clinical parameters such as latest viral load, CD4+ T-cell counts, and CD4:CD8 ratio were also significantly associated with cocaine use, depending on the statistical model used.
Based on these assessments, cocaine use seems to be associated with more severe HIV-1 disease.
*Department of Microbiology and Immunology, Drexel University College of Medicine, Philadelphia, PA;
†Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, PA;
‡Department of Biostatistics and Epidemiology, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA;
§Center for Clinical and Translational Medicine, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, PA; and
‖Division of Infectious Diseases and HIV Medicine, Department of Medicine, Drexel University College of Medicine, Philadelphia, PA.
Correspondence to: Brian Wigdahl, PhD, Department of Microbiology and Immunology, Drexel University College of Medicine, 245 North 1 Street, MS 1013A, Philadelphia, PA 19102 (e-mail: email@example.com).
Presented at the Society on NeuroImmune Pharmacology Conference, April 3, 2013, San Juan, PR.
M.R.N., V.P., and B.W. are supported in part by funds from the Public Health Service, National Institutes of Health, through grants from the National Institute of Neurological Disorders and Stroke, NS32092 and NS46263 (B.W., principal investigator), and the National Institute of Drug Abuse, DA19807 (B.W., principal investigator). M.R.N. is also supported by the National Institute of Mental Health Comprehensive NeuroAIDS Core Center (CNAC) Developmental Grant, 1P30 MH-092177-01A (M.R.N., principal investigator) and by research developmental funding provided by the Department of Microbiology and Immunology and the Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine. The remaining authors have no funding or conflicts of interest to disclose.
Received April 03, 2014
Accepted April 03, 2014