Evidence map›Paper›PMID 31631785›Full record

ArticleEmerging microbes & infections2019

GILT restricts the cellular entry mediated by the envelope glycoproteins of SARS-CoV, Ebola virus and Lassa fever virus.

Danying Chen, Zhifei Hou, Dong Jiang, Mei Zheng, Guoli Li, Yue Zhang, Rui Li, Hanxin Lin, Jinhong Chang, Hui Zeng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Emerging microbes & infections, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Cholesterol 25-hydroxylase suppresses SARS-CoV-2 replication by blocking membrane fusion.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

12 authors at 3 institutions in 3 countries.

Danying ChenInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Zhifei HouInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Dong JiangInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Mei ZhengInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Guoli LiInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Yue ZhangInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Rui LiInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Hanxin LinDepartment of Pathology and Laboratory Medicine, Western University , London , Ontario , Canada.
Jinhong ChangBaruch S. Blumberg Institute, Hepatitis B Foundation , Doylestown , PA , USA.
Hui ZengInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.
Ju-Tao GuoBaruch S. Blumberg Institute, Hepatitis B Foundation , Doylestown , PA , USA.
Xuesen ZhaoInstitute of Infectious disease, Beijing Ditan Hospital, Capital Medical University , Beijing , People's Republic of China.ORCID https://orcid.org/0000-0003-1286-5733
Capital Medical University · CNHepatitis B Foundation · USWestern University · CA

Funding

Evaulation of therapeutic benefits of HBV nucleocapsid assembly inhibitorsR01AI113267 · NIAID · DREXEL UNIVERSITY · PI DU, YANMING, GUO, JU-TAO · 2014 to 2018
$2.9M
NIAID NIH HHS R01 AI113267
6 · The paper itself

Abstract

Interferons (IFNs) control viral infections by inducing expression of IFN-stimulated genes (ISGs) that restrict distinct steps of viral replication. We report herein that gamma-interferon-inducible lysosomal thiol reductase (GILT), a lysosome-associated ISG, restricts the infectious entry of selected enveloped RNA viruses. Specifically, we demonstrated that GILT was constitutively expressed in lung epithelial cells and fibroblasts and its expression could be further induced by type II interferon. While overexpression of GILT inhibited the entry mediated by envelope glycoproteins of SARS coronavirus (SARS-CoV), Ebola virus (EBOV) and Lassa fever virus (LASV), depletion of GILT enhanced the entry mediated by these viral envelope glycoproteins. Furthermore, mutations that impaired the thiol reductase activity or disrupted the N-linked glycosylation, a posttranslational modification essential for its lysosomal localization, largely compromised GILT restriction of viral entry. We also found that the induction of GILT expression reduced the level and activity of cathepsin L, which is required for the entry of these RNA viruses in lysosomes. Our data indicate that GILT is a novel antiviral ISG that specifically inhibits the entry of selected enveloped RNA viruses in lysosomes

Indexed as

Virus InternalizationCathepsin LCell LineEbolavirusHemorrhagic Fever, EbolaHumansLassa FeverLassa virusLysosomesOxidoreductases Acting on Sulfur Group DonorsSevere Acute Respiratory SyndromeSevere acute respiratory syndrome-related coronavirusViral Envelope ProteinsVirus ReplicationCathepsin LIFI30 protein, humanOxidoreductases Acting on Sulfur Group DonorsViral Envelope ProteinsEbola virusGILTInterferon-stimulated genes (ISGs)Lassa fever virusSARS-CoV

Identifiers

PMID31631785
PMCPMC6818130
OpenAlexW2981349593

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.