Publications
Department of Medicine faculty members published more than 3,000 peer-reviewed articles in 2022.
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OBJECTIVE
Research on the role psychiatric factors in HIV disease management has yielded discrepant findings, possibly because prior studies did not include comprehensive psychiatric screeners. This study administered a validated screener to examine psychiatric correlates of highly active antiretroviral therapy (HAART) utilization and viral load.
DESIGN
Community-recruited, HIV-positive impoverished persons provided sociodemographic information, completed a Diagnostic Interview Schedule that screened for psychiatric disorders, and provided a blood sample to measure HIV disease markers.
METHODS
In this cross-sectional investigation with 227 participants, a multiple logistic regression model examined correlates of HAART utilization compared to a reference group that was eligible for (i.e. CD4(+) cell count <350 cells/μl) but not taking HAART. A multiple linear regression model examined correlates of HIV viral load among 147 participants on HAART.
RESULTS
Sleeping on the street [adjusted OR (AOR) = 0.06; 95% confidence interval (CI) = 0.01–0.26] and screening positive for a stimulant use disorder (AOR = 0.29; 95% CI = 0.13–0.65) were independently associated with lower odds of HAART utilization. Conversely, enrollment in the AIDS Drug Assistance Program (AOR = 3.94; 95% CI = 1.45–10.73) and receipt of mental health treatment (AOR = 4.78; 95% CI = 1.77–12.87) were independently associated with increased odds of HAART utilization. Among those on HAART, screening positive for a severe mental illness was independently associated with a six-fold higher viral load.
CONCLUSION
Providing psychiatric treatment could optimize health outcomes among HIV-positive impoverished persons and boost the effectiveness of 'test and treat' approaches to HIV prevention.
View on PubMed2011
BACKGROUND
Elevated immune activation persists during treated human immunodeficiency virus (HIV) infection and is associated with blunted CD4 recovery and premature mortality, but its causes remain incompletely characterized. We hypothesized that asymptomatic cytomegalovirus (CMV) replication might contribute to immune activation in this setting.
METHODS
Thirty antiretroviral therapy-treated HIV-infected CMV-seropositive participants with CD4 counts <350 cells/mm(3) were randomized to receive valganciclovir 900 mg daily or placebo for 8 weeks, followed by an additional 4-week observation period. The primary outcome was the week 8 change in percentage of activated (CD38(+) HLA-DR(+)) CD8(+) T cells.
RESULTS
Fourteen participants were randomized to valganciclovir and 16 to placebo. Most participants (21 [70%] of 30) had plasma HIV RNA levels <75 copies/mL. The median CD4 count was 190 (IQR: 134-232) cells/mm(3), and 12 (40%) of 30 had detectable CMV DNA in saliva, plasma, or semen at baseline. CMV DNA continued to be detectable at weeks 4-12 in 7 (44%) of 16 placebo-treated participants, but in none of the valganciclovir-treated participants (P = .007). Valganciclovir-treated participants had significantly greater reductions in CD8 activation at weeks 8 (P = .03) and 12 (P = .02) than did placebo-treated participants. These trends were significant even among those with undetectable plasma HIV RNA levels.
CONCLUSIONS
CMV (and/or other herpesvirus) replication is a significant cause of immune activation in HIV-infected individuals with incomplete antiretroviral therapy-mediated CD4(+) T cell recovery.
CLINICAL TRIALS REGISTRATION
NCT00264290.
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