期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 579, 期 -, 页码 141-145出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.09.024
关键词
SARS-CoV-2; DNA damage Response; Genome instability; Telomeres
资金
- University of Vermont Cancer Center summer fellowship
- DUSRA research award
- University of Vermont Office of the Vice President for Research
- University of Vermont Cancer Center Pilot project grant
- NIH [T32 AI055402]
- COBRE Pilot project grant from the Vermont Center of Immunology and Infectious Diseases
- University of Vermont Office of the Vice President for Research-Bellinger research funds
SARS-CoV-2 infection may trigger a DNA damage response in host cells, leading to telomere shortening and reduced expression of the TRF2 shelterin-protein complex.
The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus responsible for the current COVID-19 pandemic and has now infected more than 200 million people with more than 4 million deaths globally. Recent data suggest that symptoms and general malaise may continue long after the infection has ended in recovered patients, suggesting that SARS-CoV-2 infection has profound consequences in the host cells. Here we report that SARS-CoV-2 infection can trigger a DNA damage response (DDR) in African green monkey kidney cells (Vero E6). We observed a transcriptional upregulation of the Ataxia telangiectasia and Rad3 related protein (ATR) in infected cells. In addition, we observed enhanced phosphorylation of CHK1, a downstream effector of the ATR DNA damage response, as well as H2AX. Strikingly, SARS-CoV-2 infection lowered the expression of TRF2 shelterin-protein complex, and reduced telomere lengths in infected Vero E6 cells. Thus, our observations suggest SARS-CoV-2 may have pathological consequences to host cells beyond evoking an immunopathogenic immune response. (c) 2021 Elsevier Inc. All rights reserved.
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