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Cyclin D3 restricts SARS-CoV-2 envelope incorporation into virions and interferes with viral spread

Ravi K Gupta1,2,3, Petra Mlcochova1,2

  • 1Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Cambridge, UK.

The EMBO Journal
|September 26, 2022
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection degrades cyclin D3, a host protein. Depleting cyclin D3 enhances viral replication, suggesting a role in controlling SARS-CoV-2 assembly.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The COVID-19 pandemic, caused by SARS-CoV-2, highlights the need to understand host-virus interactions.
  • Host cell machinery is critical for viral replication and transmission.

Purpose of the Study:

  • To investigate the impact of SARS-CoV-2 infection on host cell cyclins.
  • To elucidate the role of specific cyclins in SARS-CoV-2 replication and assembly.

Main Methods:

  • Analyzing protein levels and localization (cyclins D1, D3) in SARS-CoV-2 infected cells.
  • Utilizing small-interfering RNA (siRNA) to knockdown cyclin D3.
  • Performing co-immunoprecipitation to identify protein interactions.

Main Results:

  • SARS-CoV-2 infection induced nuclear-to-cytoplasmic redistribution and proteasomal degradation of cyclin D1 and D3.
  • Cyclin D depletion was independent of SARS-CoV-2-induced cell cycle arrest.
  • Knockdown of cyclin D3 significantly increased progeny virus production.
  • Cyclin D3 was found to co-immunoprecipitate with SARS-CoV-2 E and M proteins.

Conclusions:

  • SARS-CoV-2 infection leads to the depletion of cyclin D3.
  • Cyclin D3 appears to inhibit the efficient assembly and release of new virions.
  • The degradation of cyclin D3 during infection may facilitate virus production.
Keywords:
FucciSARS-CoV-2assemblycell cyclecyclin D3

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