Comprehensive mapping of the signaling events evoked by SARS-CoV-2 variants delta and omicron in human astrocytes

COVID-19 causes a wide range of complications in the central nervous system, including encephalitis and other neurological symptoms such as memory problems, psychological disorders, depression, and anxiety. We present comprehensive data on the changes in gene expression levels in astrocytes infected with the Delta or Omicron variants of SARS-CoV-2. In RNA-seq data, we found 346 genes that were significantly evoked (197 up- and 149 down-regulated) in astrocytes challenged with the Omicron variant, compared to 341 evoked genes (215 up- and 126 down-regulated) in the Delta variant. A surprisingly large number of genes were exclusively evoked by Delta (82 up- and 48 downregulated) and Omicron variants (65 up and 60 downregulated). Numerous pathways, including those pertaining to the neuronal system, metabolism, response to viral infection, signal transduction, cytokine signaling, and homeostasis, were dysregulated in infected astrocytes. In this report we have dissected major pathways that are related to pathogen recognition, integrity of the BBB and glia limitans, and neurological disorders that could lead to neurological symptoms listed above. Our findings also reveal dysregulation of a large number of non-coding RNAs. The data presented here may help us better understand the role of astrocytes in the neurological disorders seen in COVID-19 patients.

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Journal
Scientific Reports
Published
2025-10-22
DOI
https://doi.org/10.1038/s41598-025-20851-8
Primary Topic
SARS-CoV-2 and COVID-19 Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Comprehensive mapping of the signaling events evoked by SARS-CoV-2 variants delta and omicron in human astrocytes

Katarína Kucková, Monika Slavíková, Boris Klempa, Punit Tyagi et al.
Scientific Reports
SARS-CoV-2 and COVID-19 Research
article

Comprehensive mapping of the signaling events evoked by SARS-CoV-2 variants delta and omicron in human astrocytes

Katarína Kucková, Monika Slavíková, Boris Klempa, Punit Tyagi, Katarína Bhide, Mangesh Bhide, Lea Talpašová
article en

Abstract

COVID-19 causes a wide range of complications in the central nervous system, including encephalitis and other neurological symptoms such as memory problems, psychological disorders, depression, and anxiety. We present comprehensive data on the changes in gene expression levels in astrocytes infected with the Delta or Omicron variants of SARS-CoV-2. In RNA-seq data, we found 346 genes that were significantly evoked (197 up- and 149 down-regulated) in astrocytes challenged with the Omicron variant, compared to 341 evoked genes (215 up- and 126 down-regulated) in the Delta variant. A surprisingly large number of genes were exclusively evoked by Delta (82 up- and 48 downregulated) and Omicron variants (65 up and 60 downregulated). Numerous pathways, including those pertaining to the neuronal system, metabolism, response to viral infection, signal transduction, cytokine signaling, and homeostasis, were dysregulated in infected astrocytes. In this report we have dissected major pathways that are related to pathogen recognition, integrity of the BBB and glia limitans, and neurological disorders that could lead to neurological symptoms listed above. Our findings also reveal dysregulation of a large number of non-coding RNAs. The data presented here may help us better understand the role of astrocytes in the neurological disorders seen in COVID-19 patients.

Scientific ReportsVol. 15(1)
Slovak Academy of Sciences (SK), University of Veterinary Medicine in Košice (SK), Biomedical Research Center of the Slovak Academy of Sciences (SK), Institute of Neuroimmunology of the Slovak Academy of Sciences (SK), Institute of Virology of the Slovak Academy of Sciences (SK), European Institute of Oncology (IT)
Ministerstvo Školství, Mládeže a Tělovýchovy, Agentúra na Podporu Výskumu a Vývoja, Vedecká Grantová Agentúra MŠVVaŠ SR a SAV, Central European Institute of Technology
Openalex Percentile: Top 64%
SARS-CoV-2 and COVID-19 Research
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