Evidence map›Paper›PMID 36042495›Full record

ArticleCell & bioscience2022

TRIM22 suppresses Zika virus replication by targeting NS1 and NS3 for proteasomal degradation.

Shulong Zu, Chunfeng Li, Lili Li, Yong-Qiang Deng, Xiang Chen, Dan Luo, Qing Ye, Yi-Jiao Huang, Xiao-Feng Li, Rong-Rong Zhang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.4field-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

22 citing papers in PubMed, 29 citations in OpenAlex.

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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

18 authors at 7 institutions in 2 countries.

Shulong Zu *Center for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100005, China.
Chunfeng Li *Institute for Immunity, Transplantation and Infection, Department of Pathology, Department of Microbiology and Immunology, Stanford University, Stanford, CA, 94305, USA.
Lili Li *Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100005, China.
Yong-Qiang Deng *State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Xiang ChenState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Dan LuoState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Qing YeState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Yi-Jiao HuangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Xiao-Feng LiState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Rong-Rong ZhangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China.
Nina SunCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100005, China.
Xianqi ZhangCenter for Systems Medicine, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100005, China.
Saba R AliyariDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
Karin Nielsen-SainesDivision of Pediatric Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA.
Jae U JungDepartment of Cancer Biology and Global Center for Pathogens Research and Human Health, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Heng YangInstitute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100005, China. yhmyt@hotmail.com.
Cheng-Feng QinState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, 100071, China. qincf@bmi.ac.cn.
Genhong ChengDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, 90095, USA. gcheng@mednet.ucla.edu.
Academy of Military Medical Sciences · CNSuzhou Institute of Systems Medicine · CNUniversity of California, Los Angeles · USChinese Academy of Medical Sciences & Peking Union Medical College · CNInstitute of Microbiology · CNCleveland Clinic Lerner College of Medicine · USStanford University · US

Funding

Genetic evolution, pathogenesis and immune responses in mother to child transmission of ZIKVR01AI140718 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, GENHONG, JUNG, JAE U · 2018 to 2022
$3.8M
NIAID NIH HHS R01 AI140718
6 · The paper itself

Abstract

backgroundRecognition of viral invasion by innate antiviral immune system triggers activation of the type I interferon (IFN-I) and proinflammatory signaling pathways. Subsequently, IFN-I induction regulates expression of a group of genes known as IFN-I-stimulated genes (ISGs) to block viral infection. The tripartite motif containing 22 (TRIM22) is an ISG with strong antiviral functions.

resultsHere we have shown that the TRIM22 has been strongly upregulated both transcriptionally and translationally upon Zika virus (ZIKV) infection. ZIKV infection is associated with a wide range of clinical manifestations in human from mild to severe symptoms including abnormal fetal brain development. We found that the antiviral function of TRIM22 plays a crucial role in counterattacking ZIKV infection. Overexpression of TRIM22 protein inhibited ZIKV growth whereas deletion of TRIM22 in host cells increased ZIKV infectivity. Mechanistically, TRIM22, as a functional E3 ubiquitin ligase, promoted the ubiquitination and degradation of ZIKV nonstructural protein 1 (NS1) and nonstructural protein 3 (NS3). Further studies showed that the SPRY domain and Ring domain of TRIM22 played important roles in protein interaction and degradation, respectively. In addition, we found that TRIM22 also inhibited other flaviviruses infection including dengue virus (DENV) and yellow fever virus (YFV).

conclusionThus, TRIM22 is an ISG with important role in host defense against flaviviruses through binding and degradation of the NS1 and NS3 proteins.

Indexed as

InfectionNonstructural proteinTRIM22UbiquitinationZika virus

Identifiers

PMID36042495
PMCPMC9429444
OpenAlexW4293569119

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.