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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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Using 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\n                      <jats:italic>Kif11<\/jats:italic>\n                      ,\n                      <jats:italic>Ccna2<\/jats:italic>\n                      , and\n                      <jats:italic>Aurkb<\/jats:italic>\n                      . We also identified the top 10 hub genes that included\n                      <jats:italic>Prc1<\/jats:italic>\n                      ,\n                      <jats:italic>Ube2c<\/jats:italic>\n                      ,\n                      <jats:italic>Ccnb2<\/jats:italic>\n                      ,\n                      <jats:italic>Ncapg<\/jats:italic>\n                      ,\n                      <jats:italic>Aurkb<\/jats:italic>\n                      ,\n                      <jats:italic>Cep55<\/jats:italic>\n                      ,\n                      <jats:italic>Mki67<\/jats:italic>\n                      ,\n                      <jats:italic>Dlgap5<\/jats:italic>\n                      ,\n                      <jats:italic>Ccna2<\/jats:italic>\n                      , and\n                      <jats:italic>Kif11.<\/jats:italic>\n                      RT-qPCR analysis for\n                      <jats:italic>Tnfa<\/jats:italic>\n                      ,\n                      <jats:italic>Il6<\/jats:italic>\n                      ,\n                      <jats:italic>Ccl2<\/jats:italic>\n                      , and\n                      <jats:italic>Ccl3<\/jats:italic>\n                      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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s42826-025-00264-4","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T10:00:41Z","timestamp":1769594441000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Transcriptomic insights into the immune dynamics of wild-type mice challenged with SARS-CoV-2 Beta variant"],"prefix":"10.1186","volume":"42","author":[{"given":"Hamid Reza","family":"Jahantigh","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amany","family":"Elsharkawy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Komal","family":"Arora","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chinonye","family":"Dim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0970-4875","authenticated-orcid":false,"given":"Mukesh","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,1,28]]},"reference":[{"issue":"3","key":"264_CR1","doi-asserted-by":"publisher","first-page":"174","DOI":"10.1097\/MCP.0000000000000953","volume":"29","author":"G Lui","year":"2023","unstructured":"Lui G, Guaraldi G. 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