1. ¹Center for Sickle Cell Disease, Howard University College of Medicine, Washington, DC, USA
2. ²Department of Biochemistry and Molecular Biology, Howard University College of Medicine, Washington, DC, USA
3. ³Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA
4. ⁴Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL, USA
5. ⁵Children's National Medical Center, CRI Center, Washington, DC, USA
6. ⁶Department of Microbiology, Howard University College of Medicine, Washington, DC, USA

Correspondence: Dr A Gartel, Department of Medicine, University of Illinois College of Medicine, 840 S. Wood, Room 1041, Chicago, IL, 60612, USA. E-mail: agartel@uic.edu; Dr S Nekhai, Center for Sickle Cell Disease, Howard University, 520 W Street, NW, Washington, DC 20059, USA. E-mail: snekhai@howard.edu

Received 22 August 2006; Revised 4 October 2006; Accepted 19 October 2006; Published online 18 December 2006.

Abstract

Human immunodeficiency virus (HIV) and hepatitis C virus (HCV) pose major public health concerns worldwide. HCV is clearly associated with the occurrence of hepatocellular carcinoma, and recently HIV infection has also been linked to the development of a multitude of cancers. Previously, we identified a novel nucleoside analog transcriptional inhibitor ARC (4-amino-6-hydrazino-7--D-ribofuranosyl-7H-pyrrolo[2,3-d]-pyrimidine-5-carboxamide) that exhibited proapoptotic and antiangiogenic properties in vitro. Here, we evaluated the effect of ARC on HIV-1 transcription and HCV replication. Using reporter assays, we found that ARC inhibited HIV-1 Tat-based transactivation in different cell systems. Also, using hepatoma cells that harbor subgenomic and full-length replicons of HCV, we found that ARC inhibited HCV replication. Together, our data indicate that ARC could be a promising candidate for the development of antiviral therapeutics against HIV and HCV.