Evidence map›Paper›PMID 26975414›Full record

ArticleVirology journal2016

Human H7N9 virus induces a more pronounced pro-inflammatory cytokine but an attenuated interferon response in human bronchial epithelial cells when compared with an epidemiologically-linked chicken H7N9 virus.

Kelvin K W To, Candy C Y Lau, Patrick C Y Woo, Susanna K P Lau, Jasper F W Chan, Kwok-Hung Chan, Anna J X Zhang, Honglin Chen, Kwok-Yung Yuen

Abstract read
In one paragraph

Article in Virology journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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

9 authors.

Kelvin K W ToDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Candy C Y LauDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Patrick C Y WooDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Susanna K P LauDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Jasper F W ChanDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Kwok-Hung ChanDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Anna J X ZhangDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Honglin ChenDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Kwok-Yung YuenDepartment of Microbiology, The University of Hong Kong, Hong Kong Special Administrative Region, China. kyyuen@hku.hk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAvian influenza virus H7N9 has jumped species barrier, causing sporadic human infections since 2013. We have previously isolated an H7N9 virus from a patient, and an H7N9 virus from a chicken in a live poultry market where the patient visited during the incubation period. These two viruses were genetically highly similar. This study sought to use a human bronchial epithelial cell line model to infer the virulence of these H7N9 viruses in humans.

methodsHuman bronchial epithelial cell line Calu-3 was infected with two H7N9 viruses (human H7N9-HU and chicken H7N9-CK), a human H5N1 virus and a human 2009 pandemic H1N1 virus. The infected cell lysate was collected at different time points post-infection for the determination of the levels of pro-inflammatory cytokines (tumor necrosis factor α [TNF-α] and interleukin 6 [IL-6]), anti-inflammatory cytokines (interleukin 10 [IL-10] and transforming growth factor beta [TGF-β]), chemokines (interleukin 8 [IL-8] and monocyte chemoattractant protein 1 [MCP-1]), and interferons (interferon β [IFN-β] and interferon lambda 1 [IFNL1]). The viral load in the cell lysate was also measured.

resultsComparison of the human and chicken H7N9 viruses showed that H7N9-HU induced significantly higher levels of TNF-α at 12 h post-infection, and significantly higher levels of IL-8 from 12 to 48 h post-infection than those of H7N9-CK. However, the level of IFNL1 was lower for H7N9-HU than that of H7N9-CK at 48 h post-infection (P < 0.001). H7N9-HU had significantly higher viral loads than H7N9-CK at 3 and 6 h post-infection. H5N1 induced significantly higher levels of TNF-α, IL-6, IL-8, IL-10 and MCP-1 than those of H7N9 viruses at 48 h post-infection. Conversely, H1N1 induced lower levels of TNF-α, IL-10, MCP-1, IFNL1 and IFN-β when compared with H7N9 viruses at the same time point.

conclusionsH7N9-HU induced higher levels of pro-inflammatory IL-6 and IL-8 and exhibited a more rapid viral replication than H7N9-CK. However, the level of antiviral IFNL1 was lower for H7N9-HU than H7N9-CK. Our results suggest that the gained properties in modulating human innate immunity by H7N9-HU transformed it to be a more virulent virus in humans than H7N9-CK.

Indexed as

AnimalsCell LineChickensCytokinesEpithelial CellsHumansInflammation MediatorsInfluenza A Virus, H7N9 SubtypeInfluenza, HumanInfluenza in BirdsInterferonsRespiratory MucosaViral LoadVirus ReplicationCytokinesInflammation MediatorsInterferonsAvian influenza virusChemokineChickenCytokineH7N9HumanIL-8InterferonInterferon lambda 1Viral load

Identifiers

PMID26975414
PMCPMC4791762

What OpenQuestion holds

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LicenceCC BY
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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.