Evidence map›Paper›PMID 37488344›Full record

ArticleCommunications biology2023

Comparative pathogenicity of SARS-CoV-2 Omicron subvariants including BA.1, BA.2, and BA.5.

Tomokazu Tamura, Daichi Yamasoba, Yoshitaka Oda, Jumpei Ito, Tomoko Kamasaki, Naganori Nao, Rina Hashimoto, Yoichiro Fujioka, Rigel Suzuki, Lei Wang and 19 more

Abstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Trial
  2. Viral syncytia evolve to resist interferon.Nature communications · 2026
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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

29 authors.

Tomokazu Tamura *Department of Microbiology and Immunology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-1395-6610
Daichi Yamasoba *Division of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoshitaka Oda *Department of Cancer Pathology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Jumpei Ito *Division of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-0440-8321
Tomoko Kamasaki *Department of Cell Physiology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Naganori Nao *Institute for Vaccine Research and Development, HU-IVReD, Hokkaido University, Sapporo, Japan.
Rina Hashimoto *Center for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.ORCID 0000-0002-7174-4563
Yoichiro FujiokaDepartment of Cell Physiology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Rigel SuzukiDepartment of Microbiology and Immunology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Lei WangDepartment of Cancer Pathology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-6145-395X
Hayato ItoDepartment of Microbiology and Immunology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Yukie KashimaGraduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Japan.
Izumi KimuraDivision of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Mai KishimotoDivision of Molecular Pathobiology, International Institute for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Masumi TsudaDepartment of Cancer Pathology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0001-5400-5905
Hirofumi SawaInstitute for Vaccine Research and Development, HU-IVReD, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-2569-2755
Kumiko YoshimatsuInstitute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0002-0062-2753
Yuki YamamotoHiLung Inc, Kyoto, Japan.
Tetsuharu NagamotoHiLung Inc, Kyoto, Japan.
Jun KanamuneHiLung Inc, Kyoto, Japan.
Yutaka SuzukiGraduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Japan.ORCID 0000-0003-4852-1879
Yusuke OhbaDepartment of Cell Physiology, Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-2461-8289
Genotype to Phenotype Japan (G2P-Japan) Consortium
Isao YokotaDepartment of Biostatistics, Faculty of Medicine, Hokkaido University, Sapporo, Japan. yokotai@pop.med.hokudai.ac.jp.ORCID 0000-0001-6254-2225
Keita MatsunoInstitute for Vaccine Research and Development, HU-IVReD, Hokkaido University, Sapporo, Japan. matsuk@czc.hokudai.ac.jp.ORCID 0000-0002-4205-6526
Kazuo TakayamaAMED-CREST, Japan Agency for Medical Research and Development (AMED), Tokyo, Japan. kazuo.takayama@cira.kyoto-u.ac.jp.ORCID 0000-0002-1132-2457
Shinya TanakaDepartment of Cancer Pathology, Faculty of Medicine, Hokkaido University, Sapporo, Japan. tanaka@med.hokudai.ac.jp.ORCID 0000-0001-6470-3301
Kei SatoDivision of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan. KeiSato@g.ecc.u-tokyo.ac.jp.ORCID 0000-0003-4431-1380
Takasuke FukuharaDepartment of Microbiology and Immunology, Faculty of Medicine, Hokkaido University, Sapporo, Japan. fukut@pop.med.hokudai.ac.jp.ORCID 0000-0001-5471-8331

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unremitting emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants necessitates ongoing control measures. Given its rapid spread, the new Omicron subvariant BA.5 requires urgent characterization. Here, we comprehensively analyzed BA.5 with the other Omicron variants BA.1, BA.2, and ancestral B.1.1. Although in vitro growth kinetics of BA.5 was comparable among the Omicron subvariants, BA.5 was much more fusogenic than BA.1 and BA.2. Airway-on-a-chip analysis showed that, among Omicron subvariants, BA.5 had enhanced ability to disrupt the respiratory epithelial and endothelial barriers. Furthermore, in our hamster model, in vivo pathogenicity of BA.5 was slightly higher than that of the other Omicron variants and less than that of ancestral B.1.1. Notably, BA.5 gains efficient virus spread compared with BA.1 and BA.2, leading to prompt immune responses. Our findings suggest that BA.5 has low pathogenicity compared with the ancestral strain but enhanced virus spread /inflammation compared with earlier Omicron subvariants.

Indexed as

COVID-19AnimalsCricetinaeInflammationSARS-CoV-2Virulence

Identifiers

PMID37488344
PMCPMC10366110

What OpenQuestion holds

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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.