Brief Report: Increased Expression of the Type I Interferon Receptor on CD4+ T Lymphocytes in HIV-1–Infected Individuals

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Type I interferons (IFN1s; eg, interferon-alpha and interferon-beta) are potent cytokines that inhibit the replication of human immunodeficiency virus-1 (HIV-1) and other viruses. The antiviral and immunoregulatory activities of IFN1 are mediated through ligand–receptor interactions with the IFN1 receptor complex (IFNAR). Variation in the cell-surface density of IFNAR could play a role in HIV-1 pathogenesis.


In this cross-sectional study of fresh whole blood, we used flow cytometry to evaluate the expression of IFNAR2 on lymphocyte subsets from HIV-1–infected (n = 33) and HIV-1–uninfected (n = 22) individuals.


In comparison with healthy blood bank donors, we observed that the HIV-1–infected individuals, particularly those having advanced to disease, exhibited the increased expression of IFNAR2 on CD4+ T cells (relative fluorescence intensity 6.9 vs. 9.0; P = 0.027). The CD4+:CD4neg T-cell IFNAR2 expression-level ratio provides an internally standardized measure of this alteration. The observed increased expression of IFNAR2 was largely restricted to CD4+ T cells that expressed the chemokine receptor CXCR4 and lacked the expression of CCR5.


HIV-1–infected individuals exhibit an increased expression of the IFN1 receptor on CD4+ T cells. The level of IFNAR2 expression seems to increase with disease progression. These findings provide insight for the immunologic alterations associated with HIV-1 infection and possibly new therapeutic approaches.

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