Open Access Research article

HIV patients treated with low-dose prednisolone exhibit lower immune activation than untreated patients

Christa Kasang1, Albrecht Ulmer2, Norbert Donhauser3, Barbara Schmidt3, August Stich4, Hartwig Klinker5, Samuel Kalluvya6, Eleni Koutsilieri1, Axel Rethwilm1 and Carsten Scheller1*

Author Affiliations

1 University of Wuerzburg, Institute of Virology und Immunobiology, 97078 Wuerzburg, Germany

2 HIV-Intensive Care Unit, Schwabstr. 26, 70197 Stuttgart, Germany

3 Institute of Virology, Clinical and Molecular Virology, National Reference Center for Retroviruses, University of Erlangen-Nuernberg, Erlangen, Germany

4 Medical Mission Institute, Department of Tropical Medicine, 97067 Wuerzburg, Germany

5 University of Wuerzburg, Medical Clinic and Policlinic II, Josef-Schneider-Str. 2, 97080 Wuerzburg, Germany

6 Bugando Medical Center, Mwanza, Tanzania

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BMC Infectious Diseases 2012, 12:14  doi:10.1186/1471-2334-12-14

Published: 20 January 2012



HIV-associated general immune activation is a strong predictor for HIV disease progression, suggesting that chronic immune activation may drive HIV pathogenesis. Consequently, immunomodulating agents may decelerate HIV disease progression.


In an observational study, we determined immune activation in HIV patients receiving low-dose (5 mg/day) prednisolone with or without highly-active antiretroviral therapy (HAART) compared to patients without prednisolone treatment. Lymphocyte activation was determined by flow cytometry detecting expression of CD38 on CD8(+) T cells. The monocyte activation markers sCD14 and LPS binding protein (LBP) as well as inflammation markers soluble urokinase plasminogen activated receptor (suPAR) and sCD40L were determined from plasma by ELISA.


CD38-expression on CD8+ T lymphocytes was significantly lower in prednisolone-treated patients compared to untreated patients (median 55.40% [percentile range 48.76-67.70] versus 73.34% [65.21-78.92], p = 0.0011, Mann-Whitney test). Similarly, we detected lower levels of sCD14 (3.6 μg/ml [2.78-5.12] vs. 6.11 μg/ml [4.58-7.70]; p = 0.0048), LBP (2.18 ng/ml [1.59-2.87] vs. 3.45 ng/ml [1.84-5.03]; p = 0.0386), suPAR antigen (2.17 μg/ml [1.65-2.81] vs. 2.56 μg/ml [2.24-4.26]; p = 0.0351) and a trend towards lower levels of sCD40L (2.70 pg/ml [1.90-4.00] vs. 3.60 pg/ml [2.95-5.30]; p = 0.0782). Viral load in both groups was similar (0.8 × 105 ng/ml [0.2-42.4 × 105] vs. 1.1 × 105 [0.5-12.2 × 105]; p = 0.3806). No effects attributable to prednisolone were observed when patients receiving HAART in combination with prednisolone were compared to patients who received HAART alone.


Patients treated with low-dose prednisolone display significantly lower general immune activation than untreated patients. Further longitudinal studies are required to assess whether treatment with low-dose prednisolone translates into differences in HIV disease progression.