Abstract
HIV replication is limited by cellular restriction factors, such as APOBEC and tetherin, which themselves are counteracted by viral proteins. SAMHD1 was recently identified as a novel HIV restriction factor in myeloid cells, and was shown to be blocked by the lentiviral protein Vpx. SAMHD1 limits viral replication through an original mechanism: it hydrolyses intracellular dNTPs in non-cycling cells, thus decreasing the amount of these key substrates, which are required for viral DNA synthesis. In this Progress article, we describe how SAMHD1 regulates the pool of intracellular nucleotides to control HIV replication and the innate immune response.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autoimmune Diseases of the Nervous System / genetics
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Deoxyribonucleotides / immunology
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Deoxyribonucleotides / metabolism
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Gene Silencing
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HIV Infections / immunology*
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HIV-1 / immunology
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HIV-1 / metabolism
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HIV-1 / pathogenicity
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HIV-1 / physiology*
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Host-Pathogen Interactions
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Humans
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Immunity, Innate / immunology
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Mice
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Monomeric GTP-Binding Proteins / chemistry
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Monomeric GTP-Binding Proteins / genetics
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Monomeric GTP-Binding Proteins / immunology*
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Monomeric GTP-Binding Proteins / metabolism
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Nervous System Malformations / genetics
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SAM Domain and HD Domain-Containing Protein 1
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Viral Regulatory and Accessory Proteins
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Virus Replication / immunology
Substances
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Deoxyribonucleotides
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VPX protein, Human immunodeficiency virus 2
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Viral Regulatory and Accessory Proteins
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SAM Domain and HD Domain-Containing Protein 1
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SAMHD1 protein, human
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Monomeric GTP-Binding Proteins
Supplementary concepts
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Aicardi-Goutieres syndrome