Open AccessActivation and inflammation markers in HIV‐1‐infected patients in dependency of treatment strategies
Author(s) -
Ehret R,
Wienbreyer A,
Obermeier M,
Baumgarten A,
Krznaric I,
Ingiliz P,
Carganico A,
Dupke S,
Cordes C,
Schulbin H,
Claus J,
Berg T
Publication year - 2012
Publication title -
journal of the international aids society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.724
H-Index - 62
ISSN - 1758-2652
DOI - 10.7448/ias.15.6.18293
Subject(s) - medicine , cd38 , cd8 , regimen , gastroenterology , viral load , inflammation , antiretroviral therapy , cohort , immunology , cd3 , immune system , human immunodeficiency virus (hiv) , genetics , stem cell , cd34 , biology
Purpose of the study HIV‐1‐infected patients have elevated levels of immune activation and systemic inflammatory markers which are partially strong predictors of disease progression or are associated with increased cardiovascular risk. The dependency of anti‐retroviral treatment (ART), the usage of NNRTI or PI‐based and the application of non‐nuc regimens is analysed here on the basis of a dataset (Chronic Inflammation Dependency on TREatment: CIDRE cohort) from 1500 patients in Berlin. Methods In a retrospective analysis we compared relative CD4+ cell counts, viral load, relative CD8+CD38+DR‐and CD3+DR+cells, concentration of high‐sensitivity C‐reactive protein (hsCRP) and interleukin‐6 (IL‐6) in therapy‐naïve or treated patients dependent on usage or non‐usage of NUCs, PI or NNRTI. Statistics were performed with R (R Core Team; 2012; R: A language and environment for statistical computing) using Wilcoxon rank sum test in two‐sided analysis. Summary of results As to expect, ART‐naïve patients (n=190) had significantly higher viral loads and lower CD4+cell counts (p: both<0.05) and showed higher activation levels than treated patient (CD8+CD38+DR‐ and CD3+DR+both<0.05). But no significant difference was calculated for hsCRP or IL‐6. Nuc‐sparing regimen (n=46) did not show any distinction compared to nuc‐containing therapies (n=1249) for the analysed parameters. Significant differences were detected for PI‐regimen (n=711) with lower CD4+ cell counts and higher activation (CD8+38+DR‐, CD3+DR+) and IL‐6 (p: all<0.05) but not for hsCRP (p=0.39). The opposite was true for NNRTI‐based therapies (n=445) with higher CD4+ cell percentages and lower activation and inflammation markers (p: all<0.05) and as well no difference in hsCRP (p=0.97) compared with all other treated patients. Conclusions The lack of differences between therapy‐naïve patients and patients on ART for inflammation markers may be due to the relative good immunological state of the first group, which could be one of the reasons why they are not treated so far. The number of nuc‐sparing regimen is perhaps too low and too undifferentiated to find diverse inflammation states. Although the differences in activation status can be attributed to different treatment strata, there is no clear explanation for this outcome. A possible reason could be a pre‐selection bias either for NNRTI‐based or PI‐based regimens. Additional data is acquired to perform longitudinal analysis to gain further insight.