Interleukin-1 receptor antagonist as a treatment of HIV infection

Abstract

The human immunodeficiency virus (HIV) apparently utilizes human chromosome 2, interleukin-1 (IL-1), glucocorticoid hormones, and viral Tat protein to accelerate its replication and the synthesis of all HIV proteins. HIV Tat protein binds to the long terminal repeat (LTR) ribonucleic acid, including the trans-acting responsive (TAR) sequence and the promoter region to increase HIV replication. Tat-TAR transactivation requires a factor encoded on the long arm of chromosome 2. The interaction of HIV with chromosome 2 may also cause the observed inhibition of interleukin-1 receptor antagonist (IL-1RA), thus increasing the production of IL-1. IL-1, in turn, stimulates the HIV-1 enhancer region of the LTR, thus increasing HIV gene expression and replication. IL-1 also induces glucocorticoid hormone synthesis which stimulates HIV in the virion infectivity factor (Vif) region, thus increasing HIV infectivity. It is, thus, proposed that IL-1RA not only may serve to inhibit HIV-induced IL-1, but may be the unidentified human chorionic gonadotropin-associated factor recently found to have anti-HIV and anti-Kaposi’s sarcoma activity.