Impaired activation of transposable elements in SARS-CoV-2 infection

Matan Sorek*, Eran Meshorer*, Sharon Schlesinger*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Emerging evidence shows that transposable elements (TEs) are induced in response to viral infections. This TE induction is suggested to trigger a robust and durable interferon response, providing a host defense mechanism. Here, we analyze TE expression changes in response to SARS-CoV-2 infection in different human cellular models. Unlike other viruses, SARS-CoV-2 infection does not lead to global upregulation of TEs in primary cells. We report a correlation between TEs activation and induction of interferon-related genes, suggesting that failure to activate TEs may account for the weak interferon response. Moreover, we identify two variables that explain most of the observed diverseness in immune responses: basal expression levels of TEs in the pre-infected cells and the viral load. Finally, analyzing the SARS-CoV-2 interactome and the epigenetic landscape around the TEs activated following infection, we identify SARS-CoV-2 interacting proteins, which may regulate chromatin structure and TE transcription. This work provides a possible functional explanation for SARS-CoV-2 success in its fight against the host immune system and suggests that TEs could serve as potential drug targets for COVID-19.

Original languageAmerican English
Article numbere55101
JournalEMBO Reports
Volume23
Issue number9
DOIs
StatePublished - 5 Sep 2022

Bibliographical note

Publisher Copyright:
© 2022 The Authors. Published under the terms of the CC BY NC ND 4.0 license.

Keywords

  • COVID-19
  • SARS-CoV-2
  • epigenetics
  • interferon response
  • transposable elements

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