Evidence map›Paper›PMID 33452423›Full record

ArticleCommunications biology2021

A risk marker of tribasic hemagglutinin cleavage site in influenza A (H9N2) virus.

Jiahao Zhang, Kaixiong Ma, Bo Li, Yiqun Chen, Ziwen Qiu, Jinchao Xing, Jinyu Huang, Chen Hu, Yifan Huang, Huanan Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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  11. Polysaccharide fromInternational journal of molecular sciences · 2024
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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

13 authors at 2 institutions in 2 countries.

Jiahao Zhang *College of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.ORCID 0000-0002-8780-1497
Kaixiong Ma *College of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Bo Li *College of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Yiqun ChenCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Ziwen QiuCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Jinchao XingCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Jinyu HuangCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.ORCID 0000-0001-8379-0770
Chen HuCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Yifan HuangCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Huanan LiCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China.
Dingxiang LiuGuangdong Province Key Laboratory of Microbial Signals and Disease Control and Integrative Microbiology Research Centre, 510642, Guangzhou, China.
Ming LiaoCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China. mliao@scau.edu.cn.
Wenbao QiCollege of Veterinary Medicine, South China Agricultural University, 510642, Guangzhou, China. qiwenbao@scau.edu.cn.ORCID 0000-0003-0610-7506
South China Agricultural University · CNKey Laboratory of Guangdong Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low pathogenic avian influenza A(H9N2) virus is endemic worldwide and continually recruit internal genes to generate human-infecting H5N1, H5N6, H7N9, and H10N8 influenza variants. Here we show that hemagglutinin cleavage sites (HACS) of H9N2 viruses tended to mutate towards hydrophilic via evolutionary transition, and the tribasic HACS were found at high prevalence in Asia and the Middle East. Our finding suggested that the tribasic H9N2 viruses increased the viral replication, stability, pathogenicity and transmission in chickens and the virulence of mice compared to the monobasic H9N2 viruses. Notably, the enlarged stem-loop structures of HACS in the RNA region were found in the increasing tribasic H9N2 viruses. The enlarged HACS RNA secondary structures of H9N2 viruses did not influence the viral replication but accelerated the frequency of nucleotide insertion in HACS. With the prevailing tendency of the tribasic H9N2 viruses, the tribasic HACS in H9N2 viruses should be paid more attention.

Indexed as

Evolution, MolecularAnimalsChickensHemagglutininsHumansInfluenza A Virus, H9N2 SubtypeMiceMutationPhylogeographyVirus ReplicationHemagglutinins

Identifiers

PMID33452423
PMCPMC7811019
OpenAlexW3125823682

What OpenQuestion holds

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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.