Evidence map›Paper›PMID 40394859›Full record

ArticleAnimal models and experimental medicine2025

Comparison of the pathogenicity of multiple SARS-CoV-2 variants in mouse models.

Qi Lv, Ming Liu, Feifei Qi, Mingya Liu, Fengdi Li, Ran Deng, Xujian Liang, Yanfeng Xu, Zhiqi Song, Yiwei Yan and 3 more

Abstract readComparative Study
In one paragraph

Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Qi LvBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.ORCID 0000-0003-2102-2877
Ming LiuBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Feifei QiBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Mingya LiuBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Fengdi LiBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Ran DengBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Xujian LiangBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Yanfeng XuBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Zhiqi SongBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Yiwei YanBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Shuyue LiBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Guocui MouBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.
Linlin BaoBeijing Key Laboratory for Animal Models of Emerging and Reemerging Infectious Diseases, NHC Key Laboratory of Comparative Medicine, Institute of Laboratory Animal Science, CAMS & PUMC, Beijing, China.ORCID 0000-0003-4869-3777

Funding

CAMS Innovation Fund for Medical Sciences 2021-I2M-1-035National Key Research and Development Program of China 2023YFF0724800National Science and Technology Infrastructure of China National Pathogen Resource Center-NPRC-32
6 · The paper itself

Abstract

backgroundNew variants of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)continue to drive global epidemics and pose significant health risks. The pathogenicity of these variants evolves under immune pressure and host factors. Understanding these changes is crucial for epidemic control and variant research.

methodsHuman angiotensin-converting enzyme 2(hACE2) transgenic mice were intranasally challenged with the original strain WH-09 and the variants Delta, Beta, and Omicron BA.1, while BALB/c mice were challenged with Omicron subvariants BA.5, BF.7, and XBB.1. To compare the pathogenicity differences among variants, we conducted a comprehensive analysis that included clinical symptom observation, measurement of viral loads in the trachea and lungs, evaluation of pulmonary pathology, analysis of immune cell infiltration, and quantification of cytokine levels.

resultsIn hACE2 mice, the Beta variant caused significant weight loss, severe lung inflammation, increased inflammatory and chemotactic factor secretion, greater macrophage and neutrophil infiltration in the lungs, and higher viral loads with prolonged shedding duration. In contrast, BA.1 showed a significant reduction in pathogenicity. The BA.5, BF.7, and XBB.1 variants were less pathogenic than the WH-09, Beta, and Delta variants when infected in BALB/c mice. This was evidenced by reduced weight loss, diminished pulmonary pathology, decreased secretion of inflammatory factors and chemokines, reduced macrophage and neutrophil infiltration, as well as lower viral loads in both the trachea and lungs.

conclusionIn hACE2 mice, the Omicron variant demonstrated the lowest pathogenicity, while the Beta variant exhibited the highest. Pathogenicity of the Delta variant was comparable to the original WH-09 strain. Among BALB/c mice, Omicron subvariants BA.5, BF.7, and XBB.1 showed no statistically significant differences in virulence.

Indexed as

COVID-19SARS-CoV-2Angiotensin-Converting Enzyme 2AnimalsCytokinesDisease Models, AnimalFemaleHumansLungMiceMice, Inbred BALB CMice, TransgenicTracheaViral LoadVirulenceACE2 protein, humanAngiotensin-Converting Enzyme 2Cytokinesmice modelpathogenicitySARS‐CoV‐2variants

Identifiers

PMID40394859
PMCPMC12431588

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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.