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Specific Immune Response to Human Immunodeficiency Virus (HIV)‐1 in Patients Assessed Through the Production of Interferon‐γ and Interleukin‐4 in HIV‐1 p24‐Activated Whole Blood Cultures: Relationship with the Viral Load in Plasma
Author(s) -
Hober,
Benyoucef,
Chieux,
D. De Groote,
De La Tribonnière,
Bocket,
Lion,
; Mouton,
Wattré
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00564.x
Subject(s) - whole blood , asymptomatic , immune system , immunology , viral load , peripheral blood mononuclear cell , cd8 , virology , antigen , medicine , interferon , virus , biology , in vitro , biochemistry
We studied the in vitro HIV‐1 antigen‐stimulated production of IFN‐γ and IL‐4 in HIV‐1‐infected patients and its relationship with viral replication as assessed through the plasma level of HIV‐1 RNA. The levels of IFN‐γ and IL‐4 were higher in supernatants of stimulated whole blood cultures than in stimulated peripheral blood mononuclear cell cultures, therefore whole blood cultures were used in the rest of the study. Specific IFN‐γ and IL‐4 responses to HIV‐1 p24 antigen were observed in HIV‐1‐infected patients but not in healthy controls ( n = 23). A lower proportion of individuals with a positive IFN‐γ response to HIV‐1 p24 was observed in patients at a declining clinical stage: 62% in asymptomatic patients (CDC group A, n = 16) versus 19% in symptomatic patients (CDC groups B and C, n = 21; P = 0.007, χ 2 testing), whereas the proportion of individuals with a positive IL‐4 response to HIV‐1 p24 was almost similar in both groups of patients (25% versus 23.8%). Increased IL‐4 production by HIV‐1 p24‐activated immunocompetent cells of patients and a predominant IL‐4 response to HIV‐1 p24 (with IL‐4/IFN‐γ > 1) were positively correlated with an increased viral load. In contrast, there was no correlation between the mitogen‐stimulated production of IL‐4 and IFN‐γ and the viral load in plasma. The CD8 T cells from whole blood of patients, but not from controls played a significant role in the HIV‐1 p24‐activated production of IFN‐γ and IL‐4. In conclusion, HIV‐1‐antigen‐stimulated whole blood appears to be a valuable tool to study the production of IL‐4 in HIV‐1‐infected patients. The cytokine profile pattern in response to epitopes of HIV‐1 gag p24 may play an important role in the host immune response to HIV‐1.