Commentary

APOBEC3G & HTLV-1: Inhibition without deamination

Klaus Strebel

• Correspondence: Klaus Strebel kstrebel@niaid.nih.gov

Author Affiliations

Laboratory of Molecular Microbiology, Viral Biochemistry Section; National Institute of Allergy and Infectious Diseases, NIH; Building 4, Room 310; 4 Center Drive, MSC 0460; Bethesda, MD 20892-0460, USA

Retrovirology 2005, 2:37 doi:10.1186/1742-4690-2-37

Published: 29 May 2005

Abstract

APOBEC3G is a cellular cytidine deaminase that was recently identified as the Vif-sensitive antiviral host factor responsible for the restriction of vif-defective HIV-1 in primary human cells and certain non-permissive T cell lines. Inhibition of HIV-1 replication is thought to be the result of APOBEC3G-induced hypermutation of the viral genome that occurs early during reverse transcription. Against this backdrop is a new report from the Uchiyama laboratory that proposes deaminase-independent restriction of HTLV-1 by APOBEC3G (Sasada et al. Retrovirology 2005, 2:32). These findings combined with recent reports of deaminase-independent inhibition of Hepatitis B virus as well as HIV-1 suggest that cytidine deaminase activity and antiviral activity may be separable functional properties of APOBEC3G.