Neuroinflammation and Modulating Factors in Depression and HIV

  • participants needed
  • sponsor
    University of Minnesota
Updated on 5 December 2022
antiretroviral therapy
depressive symptoms
depressed mood
selective serotonin reuptake inhibitors
HIV Vaccine


Determine if depression, which persists after depression treatment at 26 weeks, is associated with increased innate inflammation in a prospective cohort of HIV-infected Ugandans receiving SSRIs in which group psychotherapy is initiated.


Depression in HIV is a complex co-morbidity with both social factors such as stigma as well as biologic components. Disruptions in neurotransmitters such as serotonin and catecholamines are known to cause depression. Inflammation caused by diseases such as stroke, diabetes, and HIV is associated with higher rates of depression. HIV causes inflammation throughout the body, but since the virus can cross the blood-brain-barrier, HIV can replicate in and target the brain causing neuroinflammation which predisposes depression. However the pathophysiology of the role of inflammation in comorbid depression and HIV is poorly understood.

  1. Among depressed HIV-infected Ugandans, determine if the resolution of depression at 26 weeks of HIV therapy is improved with group psychotherapy.
  2. In the same population determine if persistent depression is associated with higher levels of innate inflammation. Also, compare baseline and follow up inflammation among depressed compared to non-depressed control group.
  3. Evaluate if viral suppression levels at 26 weeks are improved by group psychotherapy.

Condition Depression, HIV
Treatment Group Pyschotherapy, Depression Standard of Care, HIV Standard of Care
Clinical Study IdentifierNCT04286282
SponsorUniversity of Minnesota
Last Modified on5 December 2022

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