Evidence map›Paper›PMID 37161660›Full record

ArticleEmerging microbes & infections2023

Reciprocal enhancement of SARS-CoV-2 and influenza virus replication in human pluripotent stem cell-derived lung organoids

Min Jung Kim, Sumi Kim, Heeyeon Kim, Dayeon Gil, Hyeong-Jun Han, Rajesh K Thimmulappa, Jang-Hoon Choi, Jung-Hyun Kim

Open access · goldAbstract read
In one paragraph

Article in Emerging microbes & infections, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
7.5field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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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

8 authors at 3 institutions in 3 countries.

Min Jung KimDivision of Intractable Diseases Research, Department of Chronic Diseases Convergence Research, Korea National Institute of Health, Cheongju, Korea.
Sumi KimDivision of Acute Viral Disease, Center for Emerging Virus Research, National Institute of Infectious Diseases, Korea National Institute of Health, Cheongju, Korea.
Heeyeon KimDivision of Acute Viral Disease, Center for Emerging Virus Research, National Institute of Infectious Diseases, Korea National Institute of Health, Cheongju, Korea.
Dayeon GilDivision of Intractable Diseases Research, Department of Chronic Diseases Convergence Research, Korea National Institute of Health, Cheongju, Korea.
Hyeong-Jun HanDivision of Intractable Diseases Research, Department of Chronic Diseases Convergence Research, Korea National Institute of Health, Cheongju, Korea.
Rajesh K ThimmulappaDepartment of Biochemistry, Center of Excellence in Molecular Biology and Regenerative Medicine, JSS Medical College, JSS Academy of Higher Education & Research, Mysuru, India.
Jang-Hoon ChoiDivision of Acute Viral Disease, Center for Emerging Virus Research, National Institute of Infectious Diseases, Korea National Institute of Health, Cheongju, Korea.
Jung-Hyun KimDivision of Intractable Diseases Research, Department of Chronic Diseases Convergence Research, Korea National Institute of Health, Cheongju, Korea.
Korea National Institute of Health · KRNational Australia Bank · AUJSS Academy of Higher Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza A virus (FLUAV) coinfections were associated with severe respiratory failure and more deaths. Here, we developed a model for studying SARS-CoV-2 and FLUAV coinfection using human pluripotent stem cell-induced alveolar type II organoids (hiAT2). hiAT2 organoids were susceptible to infection by both viruses and had features of severe lung damage. A single virus markedly enhanced the susceptibility to other virus infections. SARS-CoV-2 delta variants upregulated α-2-3-linked sialic acid, while FLUAV upregulated angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2). Moreover, coinfection by SARS-CoV-2 and FLUAV caused hyperactivation of proinflammatory and immune-related signaling pathways and cellular damage compared to a respective single virus in hiAT2 organoids. This study provides insight into molecular mechanisms underlying enhanced infectivity and severity in patients with co-infection of SARS-CoV-2 and FLUAV, which may aid in the development of therapeutics for such co-infection cases.

Indexed as

CoinfectionCOVID-19Influenza, HumanPluripotent Stem CellsHumansLungOrganoidsSARS-CoV-2Virus ReplicationDelta variantInfluenza A virusOmicron variantSARS-CoV-2viral entry receptorWord

Identifiers

PMID37161660
PMCPMC10228311
OpenAlexW4376105877

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.