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The intensity of immune activation is linked to the level of
CCR 5 expression in human immunodeficiency virus type
1‐infected persons
Author(s) -
Portales Pierre,
Psomas Katerina Christina,
Tuaillon Edouard,
Mura Thibault,
Vendrell JeanPierre,
Eliaou JeanFrançois,
Reynes Jacques,
Corbeau Pierre
Publication year - 2012
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2012.03609.x
Subject(s) - immune system , chemokine , flow cytometry , immunology , biology , receptor , chemokine receptor , virus , virology , genetics
Summary Immune activation is a main driver of AIDS ‐ and non‐ AIDS ‐linked morbidities in the course of HIV ‐1 infection. As CCR 5, the main HIV ‐1 co‐receptor, is not only a chemokine receptor but also a co‐activation molecule expressed at the surface of T cells, it could be directly involved in this immune activation. To test this hypothesis, we measured by flow cytometry the mean number of CCR 5 molecules at the surface of non‐activated CD 4 + T cells ( CCR 5 density), which determines the intensity of CCR 5 signalling, and the percentage of CD 8 + T cells over‐expressing CD 38 ( CD 38 expression), a major marker of immune activation, in the blood of 67 HIV ‐1‐infected, non‐treated individuals. CCR 5 density was correlated with CD 38 expression independently of viral load ( P = 0·016). CCR 5 density remained unchanged after highly active anti‐retroviral therapy ( HAART ) introduction or cessation, whereas CD 38 expression decreased and increased, respectively. Moreover, pre‐therapeutic CCR 5 density was highly predictive ( r = 0·736, P < 10 −4 ) of residual CD 38 over‐expression after 9 months of HAART . Hence, CCR 5 might play an immunological role in HIV ‐1 infection as a driver of immune activation. This could explain why CCR 5 antagonists may have an inhibitory effect on immune activation.