SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses

Abstract Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By analyzing ChIP-sequencing data sets, we show that SARS-CoV-2 infection induces H3K27 acetylation of several loci within the LTR69 su...

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Main Authors: Ankit Arora, Jan Eric Kolberg, Smitha Srinivasachar Badarinarayan, Natalia Savytska, Daksha Munot, Martin Müller, Veronika Krchlíková, Daniel Sauter, Vikas Bansal
Format: Article
Language:English
Published: BMC 2023-09-01
Series:Mobile DNA
Subjects:
Online Access:https://doi.org/10.1186/s13100-023-00299-1
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author Ankit Arora
Jan Eric Kolberg
Smitha Srinivasachar Badarinarayan
Natalia Savytska
Daksha Munot
Martin Müller
Veronika Krchlíková
Daniel Sauter
Vikas Bansal
author_facet Ankit Arora
Jan Eric Kolberg
Smitha Srinivasachar Badarinarayan
Natalia Savytska
Daksha Munot
Martin Müller
Veronika Krchlíková
Daniel Sauter
Vikas Bansal
author_sort Ankit Arora
collection DOAJ
description Abstract Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By analyzing ChIP-sequencing data sets, we show that SARS-CoV-2 infection induces H3K27 acetylation of several loci within the LTR69 subfamily of ERVs. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits regulatory activity and is responsive to the transcription factors IRF3 and p65/RELA. LTR69_Dup69 is located about 500 bp upstream of a long non-coding RNA gene (ENSG00000289418) and within the PTPRN2 gene encoding a diabetes-associated autoantigen. Both ENSG00000289418 and PTPRN2 showed a significant increase in expression upon SARS-CoV-2 infection. Thus, our study sheds light on the interplay of exogenous with endogenous viruses and helps to understand how ERVs regulate gene expression during infection.
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spelling doaj.art-aff53066252f42388af9d90424d398eb2023-11-26T13:34:30ZengBMCMobile DNA1759-87532023-09-011411910.1186/s13100-023-00299-1SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retrovirusesAnkit Arora0Jan Eric Kolberg1Smitha Srinivasachar Badarinarayan2Natalia Savytska3Daksha Munot4Martin Müller5Veronika Krchlíková6Daniel Sauter7Vikas Bansal8Institute for Stem Cell Science and Regenerative MedicineInstitute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenInstitute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenGerman Center for Neurodegenerative Diseases (DZNE)Institute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenInstitute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenInstitute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenInstitute for Medical Virology and Epidemiology of Viral Diseases, University Hospital TübingenGerman Center for Neurodegenerative Diseases (DZNE)Abstract Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By analyzing ChIP-sequencing data sets, we show that SARS-CoV-2 infection induces H3K27 acetylation of several loci within the LTR69 subfamily of ERVs. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits regulatory activity and is responsive to the transcription factors IRF3 and p65/RELA. LTR69_Dup69 is located about 500 bp upstream of a long non-coding RNA gene (ENSG00000289418) and within the PTPRN2 gene encoding a diabetes-associated autoantigen. Both ENSG00000289418 and PTPRN2 showed a significant increase in expression upon SARS-CoV-2 infection. Thus, our study sheds light on the interplay of exogenous with endogenous viruses and helps to understand how ERVs regulate gene expression during infection.https://doi.org/10.1186/s13100-023-00299-1SARS-CoV-2Transposable elementsEndogenous retrovirusesSolo-LTRsLTR69
spellingShingle Ankit Arora
Jan Eric Kolberg
Smitha Srinivasachar Badarinarayan
Natalia Savytska
Daksha Munot
Martin Müller
Veronika Krchlíková
Daniel Sauter
Vikas Bansal
SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
Mobile DNA
SARS-CoV-2
Transposable elements
Endogenous retroviruses
Solo-LTRs
LTR69
title SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
title_full SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
title_fullStr SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
title_full_unstemmed SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
title_short SARS-CoV-2 infection induces epigenetic changes in the LTR69 subfamily of endogenous retroviruses
title_sort sars cov 2 infection induces epigenetic changes in the ltr69 subfamily of endogenous retroviruses
topic SARS-CoV-2
Transposable elements
Endogenous retroviruses
Solo-LTRs
LTR69
url https://doi.org/10.1186/s13100-023-00299-1
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