Abstract
Plasma levels of adenosine deaminase (ADA), an enzyme that deaminates adenosine to inosine, are increased during inflammation. An increase in ADA activity occurs with lower human immunodeficiency virus (HIV) viral load and higher CD4+ T cell counts. We aimed to investigate the role of plasma ADA as a biomarker of inflammation in treatment-naïve HIV patients who received tenofovir or another nucleoside analog for comparison. Ninety-two treatment-naïve patients were included in the study and grouped by treatment, i.e., tenofovir disoproxil fumarate (TDF), tenofovir alafenamide (TAF) or Triumeq. ADA activity was measured in plasma and cytokines were analyzed by MILLIPLEX® MAP-Luminex® Technology. Plasma concentration of monocytes and neutrophils was measured at 0, 3, and 12 months post-treatment. Treatment-naïve HIV patients had increased ADA concentrations (over 15 U/L) that decreased after treatment with TAF and Triumeq, though this did not occur in TDF-treated patients. However, all groups exhibited a pro-inflammatory systemic profile at 12 months of treatment. Plasma GM-CSF levels decreased after 12 months of treatment in the TDF group, with a concomitant decrease in blood monocyte count, and a negative correlation with ADA values was found. In conclusion, ADA levels may be modulated by antiretroviral therapy in HIV patients, possibly affecting inflammatory status.
Highlights
Complex interactions between immune cells and soluble factors are responsible for the inflammatory response triggered to protect against microorganisms or at the site of injury
We study cytokine levels and their relationship to inflammatory response after 12 months of treatment with tenofovir compositions tenofovir disoproxil fumarate (TDF) and tenofovir alafenamide (TAF) compared to another nucleoside antiretroviral drug in naïve human immunodeficiency virus (HIV) patients
In order to understand the behavior of adenosine deaminase (ADA) levels in treatment-naïve HIV patients and determine whether treatment with tenofovir modified these values, ADA concentration was evaluated at baseline and at 3 and 12 months after treatment
Summary
Complex interactions between immune cells and soluble factors are responsible for the inflammatory response triggered to protect against microorganisms or at the site of injury. One such soluble factor is adenosine, a purine nucleoside that, when accumulated in the extracellular space, modulates the immune response and prevents inflammatory tissue damage [1]. Inflammation produces an increase in extracellular adenosine, with levels reaching micromolar range [2]. These adenosine levels are regulated by a variety of mechanisms, including nucleoside transporters, intracellular and extracellular biosynthesis, and conversion to inosine by adenosine deaminase (ADA) [1]. Impaired ADA activity directly correlates with defective adenosine metabolism as shown in ADA-SCID, a severe, congenital combined immunodeficiency [3]
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