Evidence map›Paper›PMID 36532074›Full record

ArticleFrontiers in immunology2022

Interferon-inducible SAMHD1 restricts viral replication through downregulation of lipid synthesis.

Ni An, Qinghua Ge, Huihan Shao, Quanjie Li, Fei Guo, Chen Liang, Xiaoyu Li, Dongrong Yi, Long Yang, Shan Cen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  12. Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024
    Review
  13. Article
  14. Cell lipid biology in infections: an overview.Frontiers in cellular and infection microbiology · 2023
    Review
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

10 authors at 3 institutions in 2 countries.

Ni AnInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Qinghua GeInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Huihan ShaoInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Quanjie LiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Fei GuoInstitute of Pathogen Biology, Chinese Academy of Medical Science, Beijing, China.
Chen LiangLady Davis Institute for Medical Research and McGill AIDS Centre, Jewish General Hospital, Montreal, QC, Canada.
Xiaoyu LiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Dongrong YiInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Long YangResearch Center for Infectious Diseases, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Shan CenInstitute of Medicinal Biotechnology, Chinese Academy of Medical Science, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNJewish General Hospital · CATianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Type I interferon (IFN) inhibits virus infection through multiple processes. Recent evidence indicates that IFN carries out its antiviral activity through readjusting of the cellular metabolism. The sterile alpha motif and histidine-aspartate domain containing protein 1 (SAMHD1), as an interferon-stimulated gene (ISG), has been reported to inhibit a number of retroviruses and DNA viruses, by depleting dNTPs indispensable for viral DNA replication. Here we report a new antiviral activity of SAMHD1 against RNA viruses including HCV and some other flaviviruses infection. Methods: Multiple cellular and molecular biological technologies have been used to detect virus infection, replication and variation of intracellular proteins, including western blotting, qRT-PCR, Gene silencing, immunofluorescence, etc. Besides, microarray gene chip technology was applied to analyze the effects of SAMHD1 overexpression on total expressed genes. Results: Our data show that SAMHD1 down-regulates the expression of genes related to lipid bio-metabolic pathway, accompanied with impaired lipid droplets (LDs) formation, two events important for flaviviruses infection. Mechanic study reveals that SAMHD1 mainly targets on HCV RNA replication, resulting in a broad inhibitory effect on the infectivity of flaviviruses. The C-terminal domain of SAMHD1 is showed to determine its antiviral function, which is regulated by the phosphorylation of T592. Restored lipid level by overexpression of SREBP1 or supplement with LDs counteracts with the antiviral activity of SAMHD1, providing evidence supporting the role of SAMHD1-mediated down-regulation of lipid synthesis in its function to inhibit viral infection. Conclusion: SAMHD1 plays an important role in IFN-mediated blockade of flaviviruses infection through targeting lipid bio-metabolic pathway.

Indexed as

Hepatitis CInterferon Type IVirus DiseasesAntiviral AgentsDNA ReplicationDNA, ViralDown-RegulationHumansLipidsSAM Domain and HD Domain-Containing Protein 1Virus ReplicationAntiviral AgentsDNA, ViralInterferon Type ILipidsSAM Domain and HD Domain-Containing Protein 1SAMHD1 protein, humanHCVinterferonlipid droplets (LDs)SAMHD1SREBP1

Identifiers

PMID36532074
PMCPMC9755837
OpenAlexW4310546590

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.