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

Abstract: The COVID‐19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) presents a great threat to human health. The interplay between the virus and host plays a crucial role in successful virus replication and transmission. Understanding host–virus interactions are essential for the development of new COVID‐19 treatment strategies. Here, we show that SARS‐CoV‐2 infection triggers redistribution of cyclin D1 and cyclin D3 from the nucleus to the cytoplasm, followed by proteasomal degradation. No changes to other cyclins or cyclin‐dependent kinases were observed. Further, cyclin D depletion was independent of SARS‐CoV‐2‐mediated cell cycle arrest in the early S phase or S/G2/M phase. Cyclin D3 knockdown by small‐interfering RNA specifically enhanced progeny virus titres in supernatants. Finally, cyclin D3 co‐immunoprecipitated with SARS‐CoV‐2 envelope (E) and membrane (M) proteins. We propose that cyclin D3 impairs the efficient incorporation of envelope protein into virions during assembly and is depleted during SARS‐CoV‐2 infection to restore efficient assembly and release of newly produced virions.

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch

Bibliographic citation
Cyclin D3 restricts SARS‐CoV‐2 envelope incorporation into virions and interferes with viral spread ; day:10 ; month:10 ; year:2022 ; extent:15
The EMBO journal / European Molecular Biology Organization ; (10.10.2022) (gesamt 15)

Creator
Gupta, Ravi K.
Mlcochova, Petra

DOI
10.15252/embj.2022111653
URN
urn:nbn:de:101:1-2022101115141160963991
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
15.08.2025, 7:28 AM CEST

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Associated

  • Gupta, Ravi K.
  • Mlcochova, Petra

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