Cyclin D3 restricts SARS-CoV-2 envelope incorporation into virions and interferes with viral spread.
| dc.creator | Gupta, Ravi K | |
| dc.creator | Mlcochova, Petra | |
| dc.date | 2022-10-10T22:00:13Z | |
| dc.date | 2022-10-10T22:00:13Z | |
| dc.date | 2022-11-17 | |
| dc.date | 2022-05-12 | |
| dc.date | 2022-10-10T22:00:12Z | |
| dc.date.accessioned | 2026-08-03T03:12:56Z | |
| dc.description | Funder: Lister Institute of Preventive Medicine (Lister Institute); Id: http://dx.doi.org/10.13039/501100001255 | |
| dc.description | Funder: Rosetrees Trust (Rosetrees); Id: http://dx.doi.org/10.13039/501100000833 | |
| dc.description | 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. | |
| dc.format | text/xml | |
| dc.format | application/pdf | |
| dc.identifier | The EMBO Journal, article-number e111653 | |
| dc.identifier | 0261-4189 | |
| dc.identifier | embj2022111653 | |
| dc.identifier | https://www.repository.cam.ac.uk/handle/1810/341882 | |
| dc.identifier | 10.17863/CAM.89306 | |
| dc.identifier | 1460-2075 | |
| dc.identifier.uri | https://repo.dare.co.zw/handle/123456789/174114 | |
| dc.language | en | |
| dc.language | eng | |
| dc.publisher | Springer Nature | |
| dc.publisher | https://doi.org/10.15252/embj.2022111653 | |
| dc.rights | Attribution 4.0 International | |
| dc.rights | https://creativecommons.org/licenses/by/4.0/ | |
| dc.subject | Fucci | |
| dc.subject | SARS-CoV-2 | |
| dc.subject | assembly | |
| dc.subject | cell cycle | |
| dc.subject | cyclin D3 | |
| dc.subject | Humans | |
| dc.subject | SARS-CoV-2 | |
| dc.subject | Cyclin D3 | |
| dc.subject | COVID-19 | |
| dc.subject | Pandemics | |
| dc.subject | Cell Line | |
| dc.subject | Virion | |
| dc.subject | COVID-19 Drug Treatment | |
| dc.title | Cyclin D3 restricts SARS-CoV-2 envelope incorporation into virions and interferes with viral spread. | |
| dc.type | Article |