Abstract
BackgroundBoth HIV and TB cause a state of heightened immune activation. Immune activation in HIV is associated with progression to AIDS. Prior studies, focusing on persons with advanced HIV, have shown no decline in markers of cellular activation in response to TB therapy alone.MethodologyThis prospective cohort study, composed of participants within a larger phase 3 open-label randomized controlled clinical trial, measured the impact of TB treatment on immune activation in persons with non-advanced HIV infection (CD4>350 cells/mm3) and pulmonary TB. HIV load, CD4 count, and markers of immune activation (CD38 and HLA-DR on CD4 and CD8 T cells) were measured prior to starting, during, and for 6 months after completion of standard 6 month anti-tuberculosis (TB) therapy in 38 HIV infected Ugandans with smear and culture confirmed pulmonary TB.ResultsExpression of CD38, and co-expression of CD38 and HLA-DR, on CD8 cells declined significantly within 3 months of starting standard TB therapy in the absence of anti-retroviral therapy, and remained suppressed for 6 months after completion of therapy. In contrast, HIV load and CD4 count remained unchanged throughout the study period.ConclusionTB therapy leads to measurable decreases in immune activation in persons with HIV/TB co-infection and CD4 counts >350 cells/mm3.
Highlights
Cellular markers of immune activation, CD38 and HLA-DR on CD4 and CD8 T lymphocytes, are elevated in HIV infected individuals
HIV load and CD4 count remained unchanged throughout the study period
TB therapy leads to measurable decreases in immune activation in persons with HIV/TB co-infection and CD4 counts .350 cells/mm3
Summary
Cellular markers of immune activation, CD38 and HLA-DR on CD4 and CD8 T lymphocytes, are elevated in HIV infected individuals. Studies from sub-Saharan Africa have failed to see declines in HIV load after several months of TB therapy [5,6,7]. Both HIV and TB cause a state of heightened immune activation. Prior studies, focusing on persons with advanced HIV, have shown no decline in markers of cellular activation in response to TB therapy alone
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