Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
In vivo role of IL-6 on the viral load and on immunological abnormalities of HIV-infected patients.
J Acquir Immune Defic Syndr Hum Retrovirol. 1995 Jan 1;11(1):59-68. Unique Identifier : AIDSLINE MED/96130048 Marfaing-Koka A; Aubin JT; Grangeot-Keros L; Portier A; Benattar C; Merrien D; Agut H; Aucouturier P; Autran B; Wijdenes J; et al; INSERM U131, Institut Paris-Sud sur les Cytokines, Clamart,; France.
Abstract:
In vitro experiments have suggested that interleukin (IL)-6 may contribute to human immunodeficiency virus (HIV) burden and to immunological abnormalities in HIV-infected patients. We had the opportunity to directly address this question in vivo through the virological and immunological monitoring of HIV-infected patients treated with an anti-IL-6 monoclonal antibody (mAb) for a lymphoma (ANRS 018 trial). Sixteen courses of anti-IL-6 mAb administration, performed in 11 patients, were studied. All patients were at a late stage of HIV infection. The HIV load and the immunological status were determined at the initiation of each course and at its end, 21 days later. The mAb induced no significant change of HIV load, as evaluated by p24 antigenemia, plasma viremia, and quantification of circulating HIV RNA by reverse transcriptase-polymerase chain reaction and branched DNA techniques. The anti-IL-6 mAb also did not affect CD4+, CD8+, and CD19+ circulating cell counts, nor the serum concentrations of sIL-2R and of sCD8. In contrast, the mAb completely abrogated acute-phase reaction, as demonstrated by the normalization of C-reactive protein and fibrinogen circulating levels (p = 0.013 and p = 0.008, respectively). It increased serum albumin concentration. The latter effect was restricted to patients with a spontaneously low albuminemia (p = 0.01). It decreased B-lymphocyte hyperactivity, as reflected by decreased IgG and IgA serum levels (p = 0.008 and p < 0.001, respectively), and by a decreased production of IgG in vitro (p = 0.017). In contrast, the IgM hyperproduction was not affected by the mAb. Therefore, increased IL-6 production in HIV-infected patients at a late stage of the infection may not stimulate HIV replication in vivo, but it may represent a key mechanism contributing to the metabolic and immunological dysbalance of the disease.
Keywords: Acute-Phase Proteins/ANALYSIS Acute-Phase Reaction/ETIOLOGY/PHYSIOPATHOLOGY/THERAPY Antibodies, Monoclonal/ADMINISTRATION & DOSAGE/THERAPEUTIC USE Antigens, CD8/BLOOD B-Lymphocytes/IMMUNOLOGY Human HIV Core Protein p24/ANALYSIS HIV Infections/COMPLICATIONS/*IMMUNOLOGY/VIROLOGY HIV-1/*PHYSIOLOGY IgA/ANALYSIS IgG/ANALYSIS Immunophenotyping Infusions, Intravenous Interleukin-6/IMMUNOLOGY/*PHYSIOLOGY Lymphocyte Count Lymphoma, AIDS-Related/PHYSIOPATHOLOGY/THERAPY Lymphoma, High-Grade/PHYSIOPATHOLOGY/THERAPY Receptors, Interleukin-2/ANALYSIS RNA, Viral/ANALYSIS Support, Non-U.S. Gov't Viremia/PHYSIOPATHOLOGY *Virus Replication JOURNAL ARTICLE
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M9640795
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Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
