Evidence map›Paper›PMID 23231760›Full record

ArticleRetrovirology2012

SAMHD1 restricts HIV-1 infection in dendritic cells (DCs) by dNTP depletion, but its expression in DCs and primary CD4+ T-lymphocytes cannot be upregulated by interferons.

Corine St Gelais, Suresh de Silva, Sarah M Amie, Christopher M Coleman, Heather Hoy, Joseph A Hollenbaugh, Baek Kim, Li Wu

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.

0numbers the graph read from it
0cells of the map it votes in
143citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

143 citing papers in PubMed, 192 citations in OpenAlex.

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83 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Corine St GelaisCenter for Retrovirus Research, Department of Veterinary Biosciences, The Ohio State University, 1900 Coffey Road, Columbus, Ohio 43210, USA.
Suresh de Silva
Sarah M Amie
Christopher M Coleman
Heather Hoy
Joseph A Hollenbaugh
Baek Kim
Li Wu
The Ohio State University · USUniversity of Rochester · US

Funding

Replication fidelity and lentiviral pathogenesisR01AI049781 · NIAID · UNIVERSITY OF ROCHESTER · PI KIM, BAEK · 2002 to 2016
$4.9M
Training in Cellular, Biochemical and Molecular SciencesT32GM068411 · NIGMS · UNIVERSITY OF ROCHESTER · PI MAQUAT, LYNNE E · 2005 to 2019
$3.9M
SAMHD1 controls dNTP pool and HIV sensitivity to NRTIsR01GM104198 · NIGMS · UNIVERSITY OF ROCHESTER · PI KIM, BAEK · 2012 to 2018
$2.3M
The role of UBE2V1 in HIV-1 restriction in primary monocytesR21AI098524 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2012 to 2013
$419k
Novel host proteins in the HIV-1 preintegration complexesR21AI102822 · NIAID · OHIO STATE UNIVERSITY · PI WU, LI · 2012 to 2013
$406k
Replicational Fidelity and Lentivial PathogenesisR56AI049781 · NIAID · EMORY UNIVERSITY · PI KIM, BAEK · 2017 to 2017
$390k
NIAID NIH HHS AI049781NIAID NIH HHS AI098524NIAID NIH HHS AI102822NIAID NIH HHS R01 AI049781NIAID NIH HHS R21 AI102822NIGMS NIH HHS GM104198NIGMS NIH HHS R01 GM104198NIGMS NIH HHS T32 GM068411
6 · The paper itself

Abstract

backgroundSAMHD1 is an HIV-1 restriction factor in non-dividing monocytes, dendritic cells (DCs), macrophages, and resting CD4+ T-cells. Acting as a deoxynucleoside triphosphate (dNTP) triphosphohydrolase, SAMHD1 hydrolyzes dNTPs and restricts HIV-1 infection in macrophages and resting CD4+ T-cells by decreasing the intracellular dNTP pool. However, the intracellular dNTP pool in DCs and its regulation by SAMHD1 remain unclear. SAMHD1 has been reported as a type I interferon (IFN)-inducible protein, but whether type I IFNs upregulate SAMHD1 expression in primary DCs and CD4+ T-lymphocytes is unknown.

resultsHere, we report that SAMHD1 significantly blocked single-cycle and replication-competent HIV-1 infection of DCs by decreasing the intracellular dNTP pool and thereby limiting the accumulation of HIV-1 late reverse transcription products. Type I IFN treatment did not upregulate endogenous SAMHD1 expression in primary DCs or CD4+ T-lymphocytes, but did in HEK 293T and HeLa cell lines. When SAMHD1 was over-expressed in these two cell lines to achieve higher levels than that in DCs, no HIV-1 restriction was observed despite partially reducing the intracellular dNTP pool.

conclusionsOur results suggest that SAMHD1-mediated reduction of the intracellular dNTP pool in DCs is a common mechanism of HIV-1 restriction in myeloid cells. Endogenous expression of SAMHD1 in primary DCs or CD4+ T-lymphocytes is not upregulated by type I IFNs.

Indexed as

CD4-Positive T-LymphocytesDendritic CellsGene Expression RegulationHEK293 CellsHeLa CellsHIV-1HumansInterferonsMonomeric GTP-Binding ProteinsProteolysisReverse TranscriptionRNA, MessengerSAM Domain and HD Domain-Containing Protein 1Viral Regulatory and Accessory ProteinsVirus ReplicationInterferonsMonomeric GTP-Binding ProteinsRNA, MessengerSAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, humanViral Regulatory and Accessory ProteinsVPX protein, Simian immunodeficiency virus

Identifiers

PMID23231760
PMCPMC3527137
OpenAlexW2141819122

What OpenQuestion holds

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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.