Evidence map›Paper›PMID 27634893›Full record

ArticleOncotarget2016

Suppression of human metapneumovirus (HMPV) infection by the innate sensing gene CEACAM1.

Mohammad Diab, Alon Vitenshtein, Yaron Drori, Rachel Yamin, Oded Danziger, Rachel Zamostiano, Michal Mandelboim, Eran Bacharach, Ofer Mandelboim

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

9 authors at 3 institutions in 1 country.

Mohammad DiabThe Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Alon VitenshteinThe Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Yaron DroriCentral Virology Laboratory, Ministry of Health, Public Health Services, Chaim, Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel.
Rachel YaminThe Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Oded DanzigerDepartment of Cell Research and Immunology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
Rachel ZamostianoDepartment of Cell Research and Immunology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
Michal MandelboimCentral Virology Laboratory, Ministry of Health, Public Health Services, Chaim, Sheba Medical Center, Tel Hashomer, Ramat-Gan, Israel.
Eran BacharachDepartment of Cell Research and Immunology, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
Ofer MandelboimThe Lautenberg Center for General and Tumor Immunology, The BioMedical Research Institute Israel Canada of the Faculty of Medicine, The Hebrew University Hadassah Medical School, Jerusalem, Israel.
Hebrew University of Jerusalem · ILTel Aviv University · ILSheba Medical Center · IL

Funding

European Research Council 320473
6 · The paper itself

Abstract

The innate sensing system is equipped with PRRs specialized in recognizing molecular structures (PAMPs) of various pathogens. This leads to the induction of anti-viral genes and inhibition of virus growth. Human Metapneumovirus (HMPV) is a major respiratory virus that causes an upper and lower respiratory tract infection in children. In this study we show that upon HMPV infection, the innate sensing system detects the viral RNA through the RIG-I sensor leading to induction of CEACAM1 expression. We further show that CEACAM1 is induced via binding of IRF3 to the CEACAM1 promoter. We demonstrate that induction of CEACAM1 suppresses the viral loads via inhibition of the translation machinery in the infected cells in an SHP2-dependent manner. In summary, we show here that HMPV-infected cells upregulates CEACAM1 to restrict HMPV infection.

Indexed as

AnimalsAntigens, CDCell Adhesion MoleculesChlorocebus aethiopsHumansImmunity, InnateMetapneumovirusParamyxoviridae InfectionsRespiratory MucosaRespiratory Tract InfectionsUp-RegulationVero CellsAntigens, CDCD66 antigensCell Adhesion MoleculesCEACAM1HMPVImmune responseImmunityImmunology and Microbiology SectionPAMPsPRRsRIG-IRLRsSHP2

Identifiers

PMID27634893
PMCPMC5341814
OpenAlexW2519290118

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.