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SARS-CoV-2 Disrupts Splicing, Translation, and Protein Trafficking to Suppress Host Defenses

Abhik K Banerjee1, Mario R Blanco2, Emily A Bruce3

  • 1Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA; Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA.

Cell
|October 20, 2020
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host cells by targeting essential RNA processes. Viral proteins disrupt mRNA splicing, translation, and protein trafficking, ultimately suppressing the host interferon response.

Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, but its molecular pathogenesis remains unclear.
  • Understanding host-pathogen interactions is crucial for developing effective countermeasures.

Purpose of the Study:

  • To comprehensively define the interactions between SARS-CoV-2 proteins and human RNAs.
  • To elucidate the molecular mechanisms by which SARS-CoV-2 disrupts host cellular functions.

Main Methods:

  • Investigated interactions between specific SARS-CoV-2 non-structural proteins (NSPs) and human RNAs.
  • Utilized molecular biology techniques to assess the impact of these interactions on cellular processes.

Main Results:

  • NSP16 binds U1/U2 splicing RNAs, suppressing mRNA splicing.
  • NSP1 binds 18S ribosomal RNA, inhibiting mRNA translation.
  • NSP8 and NSP9 bind 7SL RNA, interfering with protein trafficking.

Conclusions:

  • SARS-CoV-2 employs a multi-pronged strategy to antagonize host cellular functions.
  • Disruption of splicing, translation, and protein trafficking suppresses the host interferon response.
  • These findings reveal key mechanisms of SARS-CoV-2 pathogenesis.
Keywords:
NSP1NSP16NSP8NSP9RNA-protein interactionsSARS-CoV-2interferonmRNA splicingprotein traffickingtranslation

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