Olorunleke Oni1, Tiffany R Glynn2, Michael H Antoni2, Danita Jemison3, Allan Rodriguez4, Mark Sharkey4, Jessica Salinas4, Mario Stevenson4, Adam W Carrico5,6. 1. Department of Family and Community Health, School of Medicine, University of Miami, Coral Gables, FL, USA. 2. Department of Psychology, College of Arts and Sciences, University of Miami, Coral Gables, FL, USA. 3. Department of Public Health Sciences, School of Medicine, University of Miami, Coral Gables, FL, USA. 4. Department of Medicine, School of Medicine, University of Miami, Coral Gables, FL, USA. 5. Department of Public Health Sciences, School of Medicine, University of Miami, Coral Gables, FL, USA. a.carrico@miami.edu. 6. University of Miami Miller School of Medicine, 1120 NW 14th Street, Office 1005, Miami, FL, 33136, USA. a.carrico@miami.edu.
Abstract
BACKGROUND: Post-traumatic stress disorder (PTSD) and stimulant use disorders are highly prevalent, commonly co-occur, and predict faster clinical HIV progression. However, scant research has examined if PTSD and cocaine use are associated with the HIV reservoir that persists in immune cells, lymphoid tissue, and organs of people living with HIV that are receiving effective treatment. METHOD: This cross-sectional study enrolled 48 HIV-positive persons with sustained undetectable viral load (< 20 copies/mL) in the past year to examine the associations of PTSD and recent cocaine use with two measures of HIV persistence in immune cells: (1) proviral HIV DNA and (2) cell-associated (CA)-HIV RNA. RESULTS: Greater PTSD symptoms were significantly associated with lower proviral HIV DNA (r = - 0.30, p = 0.041) but not with CA-HIV RNA. Greater severity of PTSD symptom clusters for intrusions (Standardized Beta = - 0.30, p = 0.038) and hyperarousal (Standardized Beta = - 0.30, p = 0.047) were independently associated with lower proviral HIV DNA. Although participants with recent cocaine use had a significantly shorter duration of sustained undetectable HIV viral load (19.9 versus 26.9 months; p = 0.047), cocaine use was not significantly associated with proviral HIV DNA or CA-HIV RNA. CONCLUSION: Further research is needed to examine the potentially bi-directional pathways linking PTSD symptom severity and HIV persistence.
BACKGROUND: Post-traumatic stress disorder (PTSD) and stimulant use disorders are highly prevalent, commonly co-occur, and predict faster clinical HIV progression. However, scant research has examined if PTSD and cocaine use are associated with the HIV reservoir that persists in immune cells, lymphoid tissue, and organs of people living with HIV that are receiving effective treatment. METHOD: This cross-sectional study enrolled 48 HIV-positive persons with sustained undetectable viral load (< 20 copies/mL) in the past year to examine the associations of PTSD and recent cocaine use with two measures of HIV persistence in immune cells: (1) proviral HIV DNA and (2) cell-associated (CA)-HIV RNA. RESULTS: Greater PTSD symptoms were significantly associated with lower proviral HIV DNA (r = - 0.30, p = 0.041) but not with CA-HIV RNA. Greater severity of PTSD symptom clusters for intrusions (Standardized Beta = - 0.30, p = 0.038) and hyperarousal (Standardized Beta = - 0.30, p = 0.047) were independently associated with lower proviral HIV DNA. Although participants with recent cocaine use had a significantly shorter duration of sustained undetectable HIV viral load (19.9 versus 26.9 months; p = 0.047), cocaine use was not significantly associated with proviral HIV DNA or CA-HIV RNA. CONCLUSION: Further research is needed to examine the potentially bi-directional pathways linking PTSD symptom severity and HIV persistence.
Entities:
Keywords:
Cocaine; HIV persistence; PTSD; Proviral HIV DNA; VACS Index
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