Evidence map›Paper›PMID 24586870›Full record

ArticlePloS one2014

SAMHD1 restricts HIV-1 replication and regulates interferon production in mouse myeloid cells.

Ruonan Zhang, Nicolin Bloch, Laura A Nguyen, Baek Kim, Nathaniel R Landau

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. IFN-JCI insight · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Incorporating alternative splicing and mRNA editing into the genetic analysis of complex traits.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Ruonan ZhangDepartment of Microbiology, NYU School of Medicine, New York, New York, United States of America.
Nicolin BlochDepartment of Microbiology, NYU School of Medicine, New York, New York, United States of America.
Laura A NguyenDepartment of Pathology, University of Rochester, Rochester, New York, United States of America.
Baek KimCenter for Drug Discovery, Department of Pediatrics, Emory School of Medicine, Atlanta, Georgia, United States of America.
Nathaniel R LandauDepartment of Microbiology, NYU School of Medicine, New York, New York, United States of America.
New York University · USCenter for Discovery · USUniversity of Rochester · US

Funding

TRAINING PROGRAM: MECHANISMS OF VIRUS-HOST INTERACTIONST32AI007647 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI Domenico Tortorella · 2000 to 2026
$11.5M
Replication fidelity and lentiviral pathogenesisR01AI049781 · NIAID · UNIVERSITY OF ROCHESTER · PI KIM, BAEK · 2002 to 2016
$4.9M
APOBEC3G/CEM15 Inhibition of Lentivirus ReplicationR01AI058864 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI LANDAU, NATHANIEL R. · 2004 to 2015
$4.5M
Vpr RevisitedR01AI067059 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI LANDAU, NATHANIEL R. · 2008 to 2017
$3.4M
NIAID NIH HHS 5R01 AI058864NIAID NIH HHS 5R01 AI067059NIAID NIH HHS AI07647NIAID NIH HHS R01 AI049781NIAID NIH HHS R01 AI058864NIAID NIH HHS R01 AI067059NIAID NIH HHS T32 AI007647
6 · The paper itself

Abstract

SAMHD1 restricts the replication of HIV-1 and other retroviruses in human myeloid and resting CD4(+) T cells and that is counteracted in SIV and HIV-2 by the Vpx accessory protein. The protein is a phosphohydrolase that lowers the concentration of deoxynucleoside triphosphates (dNTP), blocking reverse transcription of the viral RNA genome. Polymorphisms in the gene encoding SAMHD1 are associated with Aicardi-Goutières Syndrome, a neurological disorder characterized by increased type-I interferon production. SAMHD1 is conserved in mammals but its role in restricting virus replication and controlling interferon production in non-primate species is not well understood. We show that SAMHD1 is catalytically active and expressed at high levels in mouse spleen, lymph nodes, thymus and lung. siRNA knock-down of SAMHD1 in bone marrow-derived macrophages increased their susceptibility to HIV-1 infection. shRNA knock-down of SAMHD1 in the murine monocytic cell-line RAW264.7 increased its susceptibility to HIV-1 and murine leukemia virus and increased the levels of the dNTP pool. In addition, SAMHD1 knock-down in RAW264.7 cells induced the production of type-I interferon and several interferon-stimulated genes, modeling the situation in Aicardi-Goutières Syndrome. Our findings suggest that the role of SAMHD1 in restricting viruses is conserved in the mouse. The RAW264.7 cell-line serves as a useful tool to study the antiviral and innate immune response functions of SAMHD1.

Indexed as

AnimalsCell LineDNA PrimersGene Knockdown TechniquesHIV-1HumansImmunoblottingInterferon-betaLentivirusLuciferasesMiceMonomeric GTP-Binding ProteinsMyeloid CellsReal-Time Polymerase Chain ReactionRNA, Small InterferingSAM Domain and HD Domain-Containing Protein 1DNA PrimersInterferon-betaLuciferasesMonomeric GTP-Binding ProteinsRNA, Small InterferingSAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, human

Identifiers

PMID24586870
PMCPMC3929709
OpenAlexW1988261609

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.