Evidence map›Paper›PMID 36639652›Full record

ArticleCell & bioscience2023

Flavivirus prM interacts with MDA5 and MAVS to inhibit RLR antiviral signaling.

Liyan Sui, Yinghua Zhao, Wenfang Wang, Hongmiao Chi, Tian Tian, Ping Wu, Jinlong Zhang, Yicheng Zhao, Zheng-Kai Wei, Zhijun Hou and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
12.8field-weighted citation impact, top 1% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Application of Orthoflavivirus Pseudovirus Technology in Antiviral Research.International journal of molecular sciences · 2026
    Review
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  13. A review on Zika vaccine development.Pathogens and disease · 2024
    Review
  14. Article
  15. Article
  16. Review
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

14 authors at 4 institutions in 1 country.

Liyan SuiDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
Yinghua ZhaoDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
Wenfang WangCollege of Basic Medical Science, Jilin University, Changchun, China.
Hongmiao ChiCollege of Basic Medical Science, Jilin University, Changchun, China.
Tian TianCollege of Basic Medical Science, Jilin University, Changchun, China.
Ping WuCollege of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
Jinlong ZhangDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
Yicheng ZhaoDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
Zheng-Kai WeiSchool of Life Sciences and Engineering, Foshan University, Foshan, China.
Zhijun HouCollege of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
Guoqiang ZhouThe Biological safety level-3 Laboratory, Changchun Institute of Biological Products Co., Ltd, Changchun, China.
Guoqing WangCollege of Basic Medical Science, Jilin University, Changchun, China.
Zedong WangDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China. wangzedong@jlu.edu.cn.
Quan LiuDepartment of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China. liuquan1973@hotmail.com.ORCID http://orcid.org/0000-0003-3411-3196
Jilin University · CNFoshan University · CNNortheast Forestry University · CNChangchun Institute of Biological Products · CN

Funding

National Natural Science Foundation of China 81972873National Natural Science Foundation of China 82002165Pearl River Talent Plan in Guangdong Province of China 2019CX01N111
6 · The paper itself

Abstract

backgroundVector-borne flaviviruses, including tick-borne encephalitis virus (TBEV), Zika virus (ZIKV), West Nile virus (WNV), yellow fever virus (YFV), dengue virus (DENV), and Japanese encephalitis virus (JEV), pose a growing threat to public health worldwide, and have evolved complex mechanisms to overcome host antiviral innate immunity. However, the underlying mechanisms of flavivirus structural proteins to evade host immune response remain elusive.

resultsWe showed that TBEV structural protein, pre-membrane (prM) protein, could inhibit type I interferon (IFN-I) production. Mechanically, TBEV prM interacted with both MDA5 and MAVS and interfered with the formation of MDA5-MAVS complex, thereby impeding the nuclear translocation and dimerization of IRF3 to inhibit RLR antiviral signaling. ZIKV and WNV prM was also demonstrated to interact with both MDA5 and MAVS, while dengue virus serotype 2 (DENV2) and YFV prM associated only with MDA5 or MAVS to suppress IFN-I production. In contrast, JEV prM could not suppress IFN-I production. Overexpression of TBEV and ZIKV prM significantly promoted the replication of TBEV and Sendai virus.

conclusionOur findings reveal the immune evasion mechanisms of flavivirus prM, which may contribute to understanding flavivirus pathogenicity, therapeutic intervention and vaccine development.

Indexed as

FlavivirusMAVSMDA5Precursor membrane proteinRLR signaling

Identifiers

PMID36639652
PMCPMC9837762
OpenAlexW4315865716

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.