Evidence map›Paper›PMID 29346774›Full record

ArticleCell reports2018

Mannose Receptor 1 Restricts HIV Particle Release from Infected Macrophages.

Sayaka Sukegawa, Eri Miyagi, Fadila Bouamr, Helena Farkašová, Klaus Strebel

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  14. Vaginal Epithelium Transiently Harbours HIV-1 Facilitating Transmission.Frontiers in cellular and infection microbiology · 2021
    Article
  15. Review
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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 1 institution in 1 country.

Sayaka SukegawaLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 312, 4 Center Drive, MSC 0460, Bethesda, MD 20892, USA.
Eri MiyagiLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 312, 4 Center Drive, MSC 0460, Bethesda, MD 20892, USA.
Fadila BouamrLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 312, 4 Center Drive, MSC 0460, Bethesda, MD 20892, USA.
Helena FarkašováLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 312, 4 Center Drive, MSC 0460, Bethesda, MD 20892, USA.
Klaus StrebelLaboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Building 4, Room 312, 4 Center Drive, MSC 0460, Bethesda, MD 20892, USA. Electronic address: kstrebel@nih.gov.
National Institute of Allergy and Infectious Diseases · US

Funding

Molecular Analysis Of Retroviral Genes And Their ProductsZIAAI000669 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STREBEL, KLAUS · 2009 to 2025
$25.2M
Molecular Analysis Of Retroviral Genes &Their ProductsZ01AI000669 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI STREBEL, KLAUS · 1993 to 2008
$852k
Intramural NIH HHS Z01 AI000669
6 · The paper itself

Abstract

Human mannose receptor 1 (hMRC1) is expressed on the surface of most tissue macrophages, dendritic cells, and select lymphatic or liver endothelial cells. HMRC1 contributes to the binding of HIV-1 to monocyte-derived macrophages (MDMs) and is involved in the endocytic uptake of HIV-1 into these cells. Here, we identify hMRC1 as an antiviral factor that inhibits virus release through a bone marrow stromal antigen 2 (BST-2)-like mechanism. Virions produced in the presence of hMRC1 accumulated in clusters at the cell surface but were fully infectious. HIV-1 counteracted the effect by transcriptional silencing of hMRC1. The effect of hMRC1 was not virus isolate specific. Surprisingly, deletion of the Env protein, which is known to interact with hMRC1, did not relieve the hMRC1 antiviral activity, suggesting the involvement of additional cellular factor(s) in the process. Our data reveal an antiviral mechanism that is active in primary human macrophages and is counteracted by HIV-1 through downregulation of hMRC1.

Indexed as

HIV-1HumansLectins, C-TypeMacrophagesMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceVirus ReleaseLectins, C-TypeMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceHIV-1mannose receptorrestriction factorvirus release

Identifiers

PMID29346774
PMCPMC5792083
OpenAlexW2783033235

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.