Antibody to the human IFN alpha receptor reduces the loss of CD4 + T cells in macaques infected with the simian immunodeficiency virus (SIV).

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Antibody to the human IFN alpha receptor reduces the loss of CD4 + T cells in macaques infected with the simian immunodeficiency virus (SIV).

Symp Nonhum Primate Models AIDS. 1993 Sep 19-22;11:abstract no. 38. Unique Identifier : AIDSLINE PRIM11/94191632
Tovey MG; Lebon P; Meyer F; Hurtrel B; Gresser I; Venet A; Girard M; Aubertin AM; IRSC-CNRS, Villejuif, France.

Abstract: Co-factors including cytokines are thought to play a determining role in the development of the acquired immunodeficiency syndrome (AIDS) following infection by the human immunodeficiency virus (HIV). The presence of acid-labile interferon (IFN) alpha in the sera of AIDS patients has been shown to correlate with disease progression and to be of prognostic value. Alpha interferons are potent immunoregulatory molecules which enhance both T-cell and NK-cell mediated killing of virus infected cells. The abnormal production of IFN alpha in AIDS patients could enhance cytotoxicity against HIV infected cells thus contributing to the loss of CD4+ lymphocytes observed in HIV-infected individuals. To determine whether IFN alpha plays a role in the pathogenesis of AIDS we have developed an animal model based on the use of rhesus macaques infected with SIV mac. SIV is a CD4+ tropic lentivirus which shares considerable nucleotide sequence homology, antigenicity, and biologic properties with HIV. SIV-induced disease in macaques is characterized by lymphadenopathy, immune deficiency, and opportunistic infections and is considered to be an excellent experimental model of human AIDS. We have shown that infection of macaques with SIV mac is followed by a peak of serum IFN alpha at 7 to 14 days post infection which falls to undetectable levels by 21 days. The peak of serum IFN alpha occurs concomitantly with the peak of p27 antigenemia and loss of CD4+ cells, and occurs prior to the development of antibody to viral antigens. Treatment of SIV-infected macaques with a monoclonal antibody directed against the extracellular domain of the human IFN alpha receptor blocked the binding of IFN alpha to peripheral blood leukocytes, inhibited the biologic action of IFN, and markedly reduced the loss of CD4+ cells observed in SIV-infected animals. These results may have important implications for the treatment of AIDS.

Keywords: Acquired Immunodeficiency Syndrome/*BLOOD/IMMUNOLOGY Animal Antibodies, Monoclonal/*PHARMACOLOGY/THERAPEUTIC USE Antigens, CD4/*ANALYSIS Human Interferon-alpha/BLOOD Macaca Receptors, Interferon/*IMMUNOLOGY Simian Acquired Immunodeficiency Syndrome/*IMMUNOLOGY/THERAPY SIV/IMMUNOLOGY/PATHOGENICITY T-Lymphocyte Subsets/DRUG EFFECTS/*IMMUNOLOGY Time Factors ABSTRACT
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M9470886

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