IRF regulation of HIV-1 long terminal repeat activity

• Published in: Journal of interferon & cytokine research Vol. 22; no. 1; pp. 27 - 37
• Main Authors: Battistini, A, Marsili, G, Sgarbanti, M, Ensoli, B, Hiscott, J
• Format: Journal Article
• Language: English
• Published: United States 01.01.2002
• Subjects: a-Interferon; b-Interferon; Base Sequence; Cyclic AMP Response Element-Binding Protein - metabolism; DNA-Binding Proteins - physiology; Gene Expression Regulation, Viral; HIV Long Terminal Repeat; HIV-1 - genetics; HIV-1 - metabolism; Human immunodeficiency virus 1; Humans; Interferon Regulatory Factor-1; Interferon Regulatory Factor-2; interferon regulatory factors; IRF-1 protein; IRF-2 protein; Phosphoproteins - physiology; Promoter Regions, Genetic; Repressor Proteins; Response Elements; Sequence Homology; Transcription Factors - physiology; Transcriptional Activation
• ISSN: 1079-9907
• DOI: 10.1089/107999002753452638

Interferon (IFN) regulatory factors (IRF) constitute a family of transcriptional activators and repressors implicated in multiple biologic processes, including regulation of immune responses and host defense, cytokine signalling, cell growth regulation, and hematopoietic development. All members are characterized by well-conserved DNA binding domains at the N-terminal region that recognize similar DNA sequences termed IRF-binding element/IFN-stimulated response element (IRF-E/ISRE) present on the promoter of the IFN-alpha/beta genes and of some IFN-stimulated genes (ISG). Recently, a sequence homologous to the ISRE has been identified downstream of the 5' human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). This sequence is a binding site for IRF-1 and IRF-2. Deletion of the LTR-ISRE results in impaired LTR promoter activity and decreased synthesis of viral RNA and proteins. Here, we briefly summarize characteristics of IRF-1 and IRF-2 binding to the HIV-1 LTR-ISRE and the data obtained to date on the functionality of this cis-element and on the role of IRF in the regulation of HIV-1 LTR transcriptional activity.