P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication.

Husser C, Kwon H, Andersson K, Appelberg S, Montserrat N, Mirazimi A, Monteil VM

Microorganisms 12 (3) - [2024-02-22; online 2024-02-22]

While having already killed more than 7 million of people worldwide in 4 years, SARS-CoV-2, the etiological agent of COVID-19, is still circulating and evolving. Understanding the pathogenesis of the virus is of capital importance. It was shown that in vitro and in vivo infection with SARS-CoV-2 can lead to cell cycle arrest but the effect of the cell cycle arrest on the virus infection and the associated mechanisms are still unclear. By stopping cells in the G1 phase as well as targeting several pathways involved using inhibitors and small interfering RNAs, we were able to determine that the cell cycle arrest in the late G1 is beneficial for SARS-CoV-2 replication. This cell cycle arrest is independent of p53 but is dependent on the CDC25A-CDK2/cyclin E pathway. These data give a new understanding in SARS-CoV-2 pathogenesis and highlight some possible targets for the development of novel therapeutic approaches.

Category: Biochemistry

Category: Genomics & transcriptomics

Funder: H2020

Type: Journal article

PubMed 38543494

DOI 10.3390/microorganisms12030443

Crossref 10.3390/microorganisms12030443

pmc: PMC10972258
pii: microorganisms12030443

Publications 9.5.0