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Proteins can form homomeric complexes with another unit of the same protein or heteromeric complexes with different types.  Most protein complexes self-assemble spontaneously via ordered pathways, while some proteins need assembly factors that guide their proper assembly. Despite the crowded intracellular environment, proteins usually interact with their correct partners and form functional complexes.
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Human coronaviruses disassemble processing bodies.

Mariel Kleer1,2,3, Rory P Mulloy1,2,3, Carolyn-Ann Robinson1,2,3

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This summary is machine-generated.

Severe coronaviruses disrupt cellular processing bodies (PBs), leading to increased inflammatory cytokine production. The SARS-CoV-2 nucleocapsid protein specifically triggers this PB disassembly, contributing to severe COVID-19 symptoms.

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Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Dysregulated proinflammatory cytokine responses characterize severe SARS-CoV-2 infections.
  • Processing bodies (PBs) regulate innate immunity by controlling mRNA decay, including cytokine transcripts.
  • PB disassembly is linked to increased cytokine stability and translation, often induced by viruses.

Purpose of the Study:

  • To investigate the impact of human coronaviruses (CoVs) on Processing Bodies (PBs).
  • To identify the specific SARS-CoV-2 component responsible for PB disassembly.
  • To elucidate the mechanism linking SARS-CoV-2 infection to dysregulated cytokine production.

Main Methods:

  • Screening of a SARS-CoV-2 gene library.
  • Expression of viral nucleocapsid (N) proteins from various CoVs.
  • RNA fluorescent in situ hybridization to track cytokine transcripts (TNF, IL-6).
  • Microscopy to assess PB formation and disassembly.

Main Results:

  • SARS-CoV-2 and common cold CoVs (OC43, 229E) induced PB loss.
  • SARS-CoV-2 nucleocapsid (N) protein alone was sufficient to cause PB disassembly.
  • PB loss correlated with increased cytoplasmic localization of TNF and IL-6 transcripts.
  • N proteins from other human CoVs did not significantly induce PB disassembly.

Conclusions:

  • SARS-CoV-2 infection leads to Processing Body disassembly.
  • The viral nucleocapsid protein is a key driver of SARS-CoV-2-induced PB disassembly.
  • This mechanism contributes to the heightened proinflammatory cytokine production in severe COVID-19.