Evidence map›Paper›PMID 33472929›Full record

ArticleJournal of virology2021

Identification of the interferon-inducible GTPase GBP1 as major restriction factor for the Hepatitis E virus.

Mirco Glitscher, Kiyoshi Himmelsbach, Kathrin Woytinek, Anja Schollmeier, Reimar Johne, Gerrit J K Praefcke, Eberhard Hildt

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

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  7. Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024
    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

7 authors at 2 institutions in 1 country.

Mirco GlitscherDepartment Virology; Paul-Ehrlich-Institut; D-63225 Langen, Germany.
Kiyoshi HimmelsbachDepartment Virology; Paul-Ehrlich-Institut; D-63225 Langen, Germany.
Kathrin WoytinekDepartment Virology; Paul-Ehrlich-Institut; D-63225 Langen, Germany.
Anja SchollmeierDepartment Virology; Paul-Ehrlich-Institut; D-63225 Langen, Germany.
Reimar JohneDepartment Biological Safety; German Federal Institute for Risk Assessment; Berlin, D-10589 Berlin,; Germany.
Gerrit J K PraefckeDepartment Haematology and Transfusion Medicine; Paul-Ehrlich-Institut, D-63225 Langen, Hessen,; Germany.
Eberhard HildtDepartment Virology; Paul-Ehrlich-Institut; D-63225 Langen, Germany. eberhard.hildt@pei.de.ORCID https://orcid.org/0000-0002-3020-9564
Paul Ehrlich Institut · DEFederal Institute for Risk Assessment · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aims to gain deeper insight into HEV-induced innate immunity by characterizing the crosstalk between the virus and the host factor guanylate-binding protein 1 (GBP1). We observe that the amount of GBP1 is elevated upon infection, although number of transcripts is decreased, which is explained by a prolonged protein half-life. Modulation of GBP1 levels via overexpression significantly inhibits the viral life cycle. Use of various GBP-1 mutants revealed that the antiviral effect of GBP-1 on HEV is independent from the GTPase-activity, but depends on the capacity of GBP-1 to form GBP1 homodimers. This connects GBP-1 to the autophagosomal pathway. Indeed, dimerization competent GBP1 targets the viral capsid protein to the lysosomal compartment leading to inactivation of the viral particle. Most importantly, silencing of GBP1 abolishes the antiviral effect of IFNγ on HEV. In IFNγ treated cells the virus is targeted to lysosomal structures and destroyed therein. This process depends in part on GBP1. These observations about the relevance of GBP1 for type II interferon-mediated innate immunity against HEV could be a base for tailoring novel antivirals and improvement of disease management.

Identifiers

PMID33472929
PMCPMC8092694
OpenAlexW3122933575

What OpenQuestion holds

Textmetadata
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.