ArticleLaboratory animal research2026
Transcriptomic insights into the immune dynamics of wild-type mice challenged with SARS-CoV-2 Beta variant.
Article in Laboratory animal research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundMice are useful small animal models to study the pathogenesis of SARS-CoV-2 infection. As the ancestral SARS-CoV-2 strains did not utilize murine Ace2 as a receptor, wild-type mice were not susceptible to the SARS-CoV-2 infection. Infection of human ACE2-expressing transgenic mice with SARS-CoV-2 induces fatal encephalitis, which is not commonly observed in humans. We and others have previously demonstrated the ability of the SARS-CoV-2 Beta variant to productively infect wild-type mice. Herein, we employed RNA-seq to investigate the transcriptomic landscapes in the lungs after the infection of wild-type mice with SARS-CoV-2 Beta variant.
methodsWe intranasally infected 6-week-old wild-type C57BL/6J mice with the SARS-CoV-2 (B.1.351 strain) and collected lungs at 3- and 6-days post-infection for RNA-sequencing. We used the Limma-Voom package to identify differentially expressed genes (DEGs) and the fgsea package for pathway enrichment analysis. We used Cytoscape to identify hub genes and gene networks. Lastly, we employed RT-qPCR and multiplex assay to validate the RNA-seq data.
resultsUsing a cutoff of an adjusted p-value below 0.05 and an absolute log2 fold change value greater than 0.75, we identified 285 DEGs on day 3 and 46 DEGs on day 6. The canonical pathways analysis showed that several key pathways such as apoptosis and cytokine response were upregulated in the infected lungs. Protein-protein interaction analyses identified innovative target genes such as Kif11, Ccna2, and Aurkb. We also identified the top 10 hub genes that included Prc1, Ube2c, Ccnb2, Ncapg, Aurkb, Cep55, Mki67, Dlgap5, Ccna2, and Kif11. RT-qPCR analysis for Tnfa, Il6, Ccl2, and Ccl3 further validated the RNA-seq analysis. Consistent with gene expression results, we detected significantly increased protein levels of various inflammatory mediators such as IL-6, CCL2, CXCL2, and CXCL10 in the infected lungs.
conclusionsThis is the first transcriptomic analysis of the lungs of wild-type mice infected with a clinical isolate of SARS-CoV-2. Our findings provide a further understanding of the pathogenic events that occur in this mouse model of SARS-CoV-2 infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.