Evidence map›Paper›PMID 32796066›Full record

ArticleJournal of virology2020

Interferon-Inducible GTPase 1 Impedes the Dimerization of Rabies Virus Phosphoprotein and Restricts Viral Replication.

Bin Tian, Yueming Yuan, Yu Yang, Zhaochen Luo, Baokun Sui, Ming Zhou, Zhen F Fu, Ling Zhao

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2026
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  10. Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022
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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

8 authors at 2 institutions in 2 countries.

Bin Tian *State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Yueming Yuan *State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Yu YangState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Zhaochen LuoState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Baokun SuiState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Ming ZhouState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Zhen F FuState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Ling ZhaoState Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China zling604@yahoo.com.ORCID 0000-0003-0569-8105
Huazhong Agricultural University · CNUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rabies, caused by rabies virus (RABV), is an ancient zoonosis and still a major public health problem for humans, especially in developing countries. RABV can be recognized by specific innate recognition receptors, resulting in the production of hundreds of interferon-stimulated genes (ISGs), which can inhibit viral replication at different stages. Interferon-inducible GTPase 1 (IIGP1) is a mouse-specific ISG and belongs to the immunity-related GTPases (IRGs) family. IIGP is reported to constrain intracellular parasite infection by disrupting the parasitophorous vacuole membrane. However, the role of IIGP1 in restricting viral replication has not been reported. In this present study, we found that IIGP1 was upregulated in cells and mouse brains upon RABV infection. Overexpression of IIGP1 limited RABV replication in cell lines and reduced viral pathogenicity in a mouse model. Consistently, deficiency of IIGP1 enhanced RABV replication in different parts of mouse brains. Furthermore, we found that IIGP1 could interact with RABV phosphoprotein (P protein). Mutation and immunoprecipitation analyses revealed that the Y128 site of P protein is critical for its interaction with IIGP1. Further study demonstrated that this interaction impeded the dimerization of P protein and thus suppressed RABV replication. Collectively, our findings for the first reveal a novel role of IIGP1 in restricting a typical neurotropic virus, RABV, which will provide fresh insight into the function of this mouse-specific ISG.

Indexed as

AnimalsCell Line, TumorFemaleGene Expression RegulationGTP-Binding ProteinsGTP PhosphohydrolasesHEK293 CellsHost-Pathogen InteractionsHumansMiceMice, Inbred C57BLMice, KnockoutNeurogliaNeuronsPhosphoproteinsProtein MultimerizationGbp2 protein, mouseGbp5 protein, mouseGTP-Binding ProteinsGTP PhosphohydrolasesIigp1 protein, mouseMpa2 protein, mousePhosphoproteinsViral ProteinsdimerizationIIGP1P proteinrabies virus

Identifiers

PMID32796066
PMCPMC7565619
OpenAlexW3048970293

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.