Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein

Kasia Hrecka, Caili Hao, Magda Gierszewska, Selene K. Swanson, Malgorzata Kesik-Brodacka, Smita Srivastava, Laurence Florens, Michael P. Washburn and Jacek Skowronski ()
Additional contact information
Kasia Hrecka: Case School of Medicine
Caili Hao: Case School of Medicine
Magda Gierszewska: Cold Spring Harbor Laboratory
Selene K. Swanson: Stowers Institute for Medical Research
Malgorzata Kesik-Brodacka: Case School of Medicine
Smita Srivastava: Cold Spring Harbor Laboratory
Laurence Florens: Stowers Institute for Medical Research
Michael P. Washburn: Stowers Institute for Medical Research
Jacek Skowronski: Case School of Medicine

Nature, 2011, vol. 474, issue 7353, 658-661

Abstract: How macrophages avoid HIV-1 infection HIV-1 is unable to replicate efficiently in dendritic cells, the antigen-presenting tissue cells that function in both innate and adaptive immunity. Other primate lentiviruses, including HIV-2 and some simian immunodeficiency viruses, express a protein called Vpx that is able to overcome the block to replication. Two groups now report the identification of the restriction factor in dendritic cells and macrophages that is overcome by Vpx. Vpx is found to induce degradation of the protein SAMHD1. Mutations in SAMHD1 cause Aicardi–Goutières syndrome, a disorder characterized by inappropriate activation of the immune system. Knockdown of SAMHD1 increases HIV-1 replication in dendritic cells, which could be important for generating appropriate immune responses to the virus.

Date: 2011
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DOI: 10.1038/nature10195

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