SAMHD1 knockout mice: modeling retrovirus restriction in vivo
Center for Retrovirus Research, Department of Veterinary Bioscience, 1900 Coffey Road, Columbus, OH, 43210, USA
Department of Microbial Infection and Immunity, Columbus, OH, 43210, USA
Comprehensive Cancer Center, The Ohio State University, Columbus, OH, 43210, USA
Retrovirology 2013, 10:142 doi:10.1186/1742-4690-10-142Published: 20 November 2013
The host dNTP hydrolase SAMHD1 acts as a viral restriction factor to inhibit the replication of several retroviruses and DNA viruses in non-cycling human immune cells. However, understanding the physiological role of mammalian SAMHD1 has been elusive due to the lack of an animal model. Two recent studies reported the generation of samhd1 knockout mouse models for investigating the restriction of HIV-1 vectors and endogenous retroviruses in vivo. Both studies suggest that SAMHD1 is important for regulating the intracellular dNTP pool and the intrinsic immunity against retroviral infection, despite different outcomes of HIV-1 vector transduction in these mouse models. Here I discuss the significance of these new findings and the future directions in studying SAMHD1-mediated retroviral restriction.