RT Journal Article
SR Electronic
T1 SARS-CoV-2 infection activates endogenous retroviruses of the LTR69 subfamily
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2023.03.21.533610
DO 10.1101/2023.03.21.533610
A1 Ankit Arora
A1 Jan Eric Kolberg
A1 Smitha Srinivasachar Badarinarayan
A1 Daksha Munot
A1 Martin Müller
A1 Daniel Sauter
A1 Vikas Bansal
YR 2023
UL http://biorxiv.org/content/early/2023/03/21/2023.03.21.533610.abstract
AB Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By combining RNA- and ChIP-sequencing analyses with RT-qPCR, we show that SARS-CoV-2 infection induces the LTR69 subfamily of ERVs, both in vitro and in vivo. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits enhancer 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.Competing Interest StatementThe authors have declared no competing interest.