Evidence map›Paper›PMID 36687316›Full record

ArticleiScience2023

Non-Omicron breakthrough infection with higher viral load and longer vaccination-infection interval improves SARS-CoV-2 BA.4/5 neutralization.

Sho Miyamoto, Takeshi Arashiro, Akira Ueno, Takayuki Kanno, Shinji Saito, Harutaka Katano, Shun Iida, Akira Ainai, Seiya Ozono, Takuya Hemmi and 9 more

Abstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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  6. Infectious virus shedding duration reflects secretory IgA antibody response latency after SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

19 authors.

Sho MiyamotoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Takeshi ArashiroDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Akira UenoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Takayuki KannoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Shinji SaitoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Harutaka KatanoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Shun IidaDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Akira AinaiDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Seiya OzonoDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Takuya HemmiDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Yuichiro HirataDepartment of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Saya MoriyamaResearch Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Ryutaro KotakiResearch Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Hitomi KinoshitaDepartment of Virology I, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Souichi YamadaDepartment of Virology I, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Masaharu ShinkaiTokyo Shinagawa Hospital, Tokyo 140-8522, Japan.
Shuetsu FukushiDepartment of Virology I, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Yoshimasa TakahashiResearch Center for Drug and Vaccine Development, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.
Tadaki SuzukiDepartment of Virology I, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune responses to SARS-CoV-2 variants in COVID-19 cases are influenced by various factors including pre-existing immunity via vaccination and prior infection. Elucidating the drivers for upgrading neutralizing activity to SARS-CoV-2 in COVID-19 cases with pre-existing immunity will aid in improving COVID-19 booster vaccines with enhanced cross-protection against antigenically distinct variants, including the Omicron sub-lineage BA.4/5. This study revealed that the magnitude and breadth of neutralization activity to SARS-CoV-2 variants after breakthrough infections are determined primarily by upper respiratory viral load and vaccination-infection time interval. Extensive neutralizing breadth, covering even the most antigenically distant BA.4/5, was observed in cases with higher viral load and longer time intervals. Antigenic cartography depicted a critical role of the time interval in expanding the breadth of neutralization to SARS-CoV-2 variants. Our results illustrate the importance of dosing interval optimization as well as antigen design in developing variant-proof booster vaccines.

Indexed as

Immune responseImmunologyVirology

Identifiers

PMID36687316
PMCPMC9837220

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.