Evidence map›Paper›PMID 24200852›Full record

ArticleThe American journal of pathology2014

Histopathological evaluation of the diversity of cells susceptible to H5N1 virulent avian influenza virus.

Haru Ogiwara, Fumihiko Yasui, Keisuke Munekata, Asako Takagi-Kamiya, Tsubasa Munakata, Namiko Nomura, Futoshi Shibasaki, Kazuhiko Kuwahara, Nobuo Sakaguchi, Yoshihiro Sakoda and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2014. 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
1.2field-weighted citation impact, top 20% 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, 29 citations in OpenAlex.

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  13. Transmission of HBV DNA Mediated by Ceramide-Triggered Extracellular Vesicles.Cellular and molecular gastroenterology and hepatology · 2017
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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

12 authors at 3 institutions in 1 country.

Haru OgiwaraDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Fumihiko YasuiDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Keisuke MunekataDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Asako Takagi-KamiyaDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tsubasa MunakataDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Namiko NomuraDepartment of Molecular Medical Research, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Futoshi ShibasakiDepartment of Molecular Medical Research, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Kazuhiko KuwaharaDepartment of Immunology, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.
Nobuo SakaguchiDepartment of Immunology, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.
Yoshihiro SakodaLaboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
Hiroshi KidaLaboratory of Microbiology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
Michinori KoharaDepartment of Microbiology and Cell Biology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan. Electronic address: kohara-mc@igakuken.or.jp.
Tokyo Metropolitan Institute of Medical Science · JPHokkaido University · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients infected with highly pathogenic avian influenza A H5N1 viruses (H5N1 HPAIV) show diffuse alveolar damage. However, the temporal progression of tissue damage and repair after viral infection remains poorly defined. Therefore, we assessed the sequential histopathological characteristics of mouse lung after intranasal infection with H5N1 HPAIV or H1N1 2009 pandemic influenza virus (H1N1 pdm). We determined the amount and localization of virus in the lung through IHC staining and in situ hybridization. IHC used antibodies raised against the virus protein and antibodies specific for macrophages, type II pneumocytes, or proliferating cell nuclear antigen. In situ hybridization used RNA probes against both viral RNA and mRNA encoding the nucleoprotein and the hemagglutinin protein. H5N1 HPAIV infection and replication were observed in multiple lung cell types and might result in rapid progression of lung injury. Both type II pneumocytes and macrophages proliferated after H5N1 HPAIV infection. However, the abundant macrophages failed to block the viral attack, and proliferation of type II pneumocytes failed to restore the damaged alveoli. In contrast, mice infected with H1N1 pdm exhibited modest proliferation of type II pneumocytes and macrophages and slight alveolar damage. These results suggest that the virulence of H5N1 HPAIV results from the wide range of cell tropism of the virus, excessive virus replication, and rapid development of diffuse alveolar damage.

Indexed as

Alveolar Epithelial CellsAnimalsDisease Models, AnimalImmunohistochemistryInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H5N1 SubtypeIn Situ HybridizationMacrophagesMiceMice, Inbred BALB COrthomyxoviridae InfectionsPneumonia, ViralVirus Replication

Identifiers

PMID24200852
PMCPMC3873492
OpenAlexW2059272506

What OpenQuestion holds

Textmetadata
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.