Evidence map›Paper›PMID 27892498›Full record

ArticleScientific reports2016

Sensitization with vaccinia virus encoding H5N1 hemagglutinin restores immune potential against H5N1 influenza virus.

Fumihiko Yasui, Yasushi Itoh, Ai Ikejiri, Masahiro Kitabatake, Nobuo Sakaguchi, Keisuke Munekata, Shintaro Shichinohe, Yukiko Hayashi, Hirohito Ishigaki, Misako Nakayama and 4 more

Abstract read

PubMed Full text at PMC Publisher

In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it

0cells of the map it votes in

5citing papers in PubMed

–field-weighted citation impact

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

5 citing papers in PubMed.

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.

Fumihiko YasuiDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Yasushi ItohDivision of Pathology and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Setatsukinowa, Otsu, Shiga 520-2192, Japan.

Ai IkejiriDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Masahiro KitabatakeDepartment of Immunology, Nara Medical University, 840 Shijyomachi, Kashihara, Nara 634-8521, Japan.

Nobuo SakaguchiDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Keisuke MunekataDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Shintaro ShichinoheDivision of Pathology and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Setatsukinowa, Otsu, Shiga 520-2192, Japan.

Yukiko HayashiDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Hirohito IshigakiDivision of Pathology and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Setatsukinowa, Otsu, Shiga 520-2192, Japan.

Misako NakayamaDivision of Pathology and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Setatsukinowa, Otsu, Shiga 520-2192, Japan.

Yoshihiro SakodaLaboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido 060-0818, Japan.

Hiroshi KidaLaboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido 060-0818, Japan.

Kazumasa OgasawaraDivision of Pathology and Disease Regulation, Department of Pathology, Shiga University of Medical Science, Setatsukinowa, Otsu, Shiga 520-2192, Japan.

Michinori KoharaDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, 2-1-6, Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

H5N1 highly pathogenic avian influenza (H5N1 HPAI) virus causes elevated mortality compared with seasonal influenza viruses like H1N1 pandemic influenza (H1N1 pdm) virus. We identified a mechanism associated with the severe symptoms seen with H5N1 HPAI virus infection. H5N1 HPAI virus infection induced a decrease of dendritic cell number in the splenic extrafollicular T-cell zone and impaired formation of the outer layers of B-cell follicles, resulting in insufficient levels of antibody production after infection. However, in animals vaccinated with a live recombinant vaccinia virus expressing the H5 hemagglutinin, infection with H5N1 HPAI virus induced parafollicular dendritic cell accumulation and efficient antibody production. These results indicate that a recombinant vaccinia encoding H5 hemagglutinin gene does not impair dendritic cell recruitment and can be a useful vaccine candidate.

Indexed as

AnimalsB-LymphocytesCD11c AntigenDendritic CellsFemaleHemagglutinin Glycoproteins, Influenza VirusHost-Pathogen InteractionsImmunity, HumoralInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeInfluenza VaccinesLungMacaca fascicularisMice, Inbred BALB COrthomyxoviridae InfectionsPneumonia, ViralCD11c Antigenhemagglutinin, avian influenza A virusHemagglutinin Glycoproteins, Influenza VirusInfluenza Vaccines

Identifiers

PMID27892498

DOI10.1038/srep37915

PMCPMC5124960

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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.