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Impaired phagocytosis among patients infected by the human immunodeficiency virus: implication for a role of highly active anti‐retroviral therapy
Author(s) -
Michailidis C.,
Giannopoulos G.,
Vigklis V.,
Armenis K.,
Tsakris A.,
Gargalianos P.
Publication year - 2012
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2011.04526.x
Subject(s) - respiratory burst , immunology , phagocytosis , monocyte , viral load , immunity , biology , virus , immune system , virology , medicine
Summary In patients with human immunodeficiency virus (HIV) infection, neutrophil and monocyte functions, including phagocytosis, are impaired. The purpose of this study was to investigate changes of phagocytic function and respiratory burst occurring over the course of patients infected by the HIV‐1 virus. Treatment‐naive patients (group B), patients receiving highly active anti‐retroviral treatment (HAART) (group C) and patients in which HAART has failed (group D) were studied and compared with healthy volunteers (group A). Phagocytosis and oxidative burst were evaluated using commercially available kits. Results clearly denote a significant decrease of the phagocytic function of both cell types of groups B and C compared with group A. Among group C patients, those in the upper quartile of CD4 increase had higher oxidative burst compared with patients of the other quartiles. In addition, comparisons clearly showed a lower degree of phagocytic function and of oxidative burst of both monocytes and neutrophils of group D compared with group B. Finally, it was found that monocyte and neutrophil function was correlated inversely to the change in viral load, i.e. the greater the decrease of viral load, the better the phagocytic and oxidative activity. Innate immunity defects appear to be present in HIV‐positive patients, regarding phagocytic activity and oxidative burst of monocytes and neutrophils. These defects are greatly influenced by the level of treatment efficacy, with emphasis on CD4 cell counts and viral load.

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