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

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...

Full description

Saved in:
Bibliographic Details
Published in:Microorganisms (Basel) 2024-02, Vol.12 (3), p.443
Main Authors: Husser, Clara, Kwon, Hyesoo, Andersson, Klara, Appelberg, Sofia, Montserrat, Nuria, Mirazimi, Ali, Monteil, Vanessa M
Format: Article
Language:English
Subjects:
Antibodies
CDK2
Cell cycle
Cell division
coronavirus
COVID-19
Cyclin E
Cyclin-dependent kinases
Flow cytometry
G1 phase
Infections
Kinases
Medicin och hälsovetenskap
Membranes
p53 Protein
Pathogenesis
pathogenicity
Physiological aspects
Proteins
Reagents
Replication
RNA
Severe acute respiratory syndrome coronavirus 2
Stem cells
Viral diseases
Virus research
Viruses
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:2076-2607
2076-2607
DOI:10.3390/microorganisms12030443