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  • team
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  • center
  • program_project
  • nrc
  • whocc
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  • software
  • tool
  • patent
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  • Assistant Professor
  • Associate Professor
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  • Clinical Research Nurse
  • Clinician Researcher
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  • Dual-education Student
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  • Lab assistant
  • Master Student
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  • Pharmacist
  • PhD Student
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  • Post-doc
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  • Research Associate
  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
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Published in EMBO reports - 16 Dec 2021

Singh M, Chazal M, Quarato P, Bourdon L, Malabat C, Vallet T, Vignuzzi M, van der Werf S, Behillil S, Donati F, Sauvonnet N, Nigro G, Bourgine M, Jouvenet N, Cecere G,

Link to Pubmed [PMID] – 34914162

Link to DOI – 10.15252/embr.202154341

EMBO Rep 2021 Dec; (): e54341

SARS-CoV-2 infection results in impaired interferon response in patients with severe COVID-19. However, how SARS-CoV-2 interferes with host immune responses is incompletely understood. Here, we sequence small RNAs from SARS-CoV-2-infected human cells and identify a microRNA (miRNA) derived from a recently evolved region of the viral genome. We show that the virus-derived miRNA produces two miRNA isoforms in infected cells by the enzyme Dicer, which are loaded into Argonaute proteins. Moreover, the predominant miRNA isoform targets the 3’UTR of interferon-stimulated genes and represses their expression in a miRNA-like fashion. Finally, the two viral miRNA isoforms were detected in nasopharyngeal swabs from COVID-19 patients. We propose that SARS-CoV-2 can potentially employ a virus-derived miRNA to hijack the host miRNA machinery, which could help to evade the interferon-mediated immune response.