ArticleNature2011
SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx.
Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 996 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
996 citing papers in PubMed, 1,477 citations in OpenAlex.
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- The Role of SAMHD1 in Viral Resistance and Transduction Efficiency Challenges in Pediatric Hematological Malignancies: Mechanistic Insights and Clinical Perspectives.European journal of haematology · 2026Review
- Transition Metal Activation Reframes SAMHD1 Regulation.ACS chemical biology · 2026Article
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- Mucosal Dynamics Contributing to Innate Immune Responses to HIV in the Human Female Genital Tract.Viruses · 2026Review
- Bioinspired oxidized mRNA lipid nanoparticles for ex vivo engineering of chimeric antigen receptor macrophages targeting solid tumors.Bioengineering & translational medicine · 2026Article
- Equine infectious anemia virus blocks interferon responses through Rev-mediated activation of the stress granule-PKR-eIF2α pathway.PLoS pathogens · 2026Article
- Transition metal activation reframes SAMHD1 regulation.bioRxiv : the preprint server for biology · 2026Article
936 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The primate lentivirus auxiliary protein Vpx counteracts an unknown restriction factor that renders human dendritic and myeloid cells largely refractory to HIV-1 infection. Here we identify SAMHD1 as this restriction factor. SAMHD1 is a protein involved in Aicardi-Goutières syndrome, a genetic encephalopathy with symptoms mimicking congenital viral infection, that has been proposed to act as a negative regulator of the interferon response. We show that Vpx induces proteasomal degradation of SAMHD1. Silencing of SAMHD1 in non-permissive cell lines alleviates HIV-1 restriction and is associated with a significant accumulation of viral DNA in infected cells. Concurrently, overexpression of SAMHD1 in sensitive cells inhibits HIV-1 infection. The putative phosphohydrolase activity of SAMHD1 is probably required for HIV-1 restriction. Vpx-mediated relief of restriction is abolished in SAMHD1-negative cells. Finally, silencing of SAMHD1 markedly increases the susceptibility of monocytic-derived dendritic cells to infection. Our results demonstrate that SAMHD1 is an antiretroviral protein expressed in cells of the myeloid lineage that inhibits an early step of the viral life cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.