Evidence map›Paper›PMID 28196963›Full record

ArticlemBio2017

Genetic Predisposition To Acquire a Polybasic Cleavage Site for Highly Pathogenic Avian Influenza Virus Hemagglutinin.

Naganori Nao, Junya Yamagishi, Hiroko Miyamoto, Manabu Igarashi, Rashid Manzoor, Aiko Ohnuma, Yoshimi Tsuda, Wakako Furuyama, Asako Shigeno, Masahiro Kajihara and 3 more

Open access · goldAbstract read
In one paragraph

Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
10.0field-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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.

  1. Pooled it
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  18. Mechanisms of COVID-19 pathogenesis in diabetes.American journal of physiology. Heart and circulatory physiology · 2022
    Review
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21 more citing papers are in PubMed but not listed here.

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.

Naganori NaoDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Junya YamagishiDivision of Collaboration and Education, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Hiroko MiyamotoDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Manabu IgarashiDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Rashid ManzoorDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Aiko OhnumaAdministration Office, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Yoshimi TsudaDepartment of Microbiology, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Wakako FuruyamaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Asako ShigenoDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Masahiro KajiharaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Noriko KishidaInfluenza Virus Research Center, National Institute of Infectious Diseases, Musashimurayama, Japan.
Reiko YoshidaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Ayato TakadaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan atakada@czc.hokudai.ac.jp.
Hokkaido University · JPNational Institute of Infectious Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Highly pathogenic avian influenza viruses with H5 and H7 hemagglutinin (HA) subtypes evolve from low-pathogenic precursors through the acquisition of multiple basic amino acid residues at the HA cleavage site. Although this mechanism has been observed to occur naturally only in these HA subtypes, little is known about the genetic basis for the acquisition of the polybasic HA cleavage site. Here we show that consecutive adenine residues and a stem-loop structure, which are frequently found in the viral RNA region encoding amino acids around the cleavage site of low-pathogenic H5 and H7 viruses isolated from waterfowl reservoirs, are important for nucleotide insertions into this RNA region. A reporter assay to detect nontemplated nucleotide insertions and deep-sequencing analysis of viral RNAs revealed that an increased number of adenine residues and enlarged stem-loop structure in the RNA region accelerated the multiple adenine and/or guanine insertions required to create codons for basic amino acids. Interestingly, nucleotide insertions associated with the HA cleavage site motif were not observed principally in the viral RNA of other subtypes tested (H1, H2, H3, and H4). Our findings suggest that the RNA editing-like activity is the key mechanism for nucleotide insertions, providing a clue as to why the acquisition of the polybasic HA cleavage site is restricted to the particular HA subtypes.

Indexed as

Genetic Predisposition to DiseaseAdenineAnimalsChickensGuanineHemagglutinin Glycoproteins, Influenza VirusHigh-Throughput Nucleotide SequencingInfluenza A Virus, H5N1 SubtypeInfluenza in BirdsRNA, ViralVirulenceAdenineGuaninehemagglutinin, avian influenza A virusHemagglutinin Glycoproteins, Influenza VirusRNA, Viral

Identifiers

PMID28196963
PMCPMC5312086
OpenAlexW2587966246

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.