AI Article Synopsis
- The study examines how SARS-CoV-2, the virus causing COVID-19, affects the stiffness of host cell cortical actin, which plays a role in cell structure and function.
- It finds that the viral Spike protein's receptor-binding domain (RBD) reduces cortical stiffness in cells that express the ACE2 receptor, leading to inactivation of key regulatory proteins (ERM).
- Additionally, different Omicron variants (BA.1 and BA.5) were shown to impact cortical stiffness based on how strongly they bind to ACE2, revealing new insights into the mechanobiological effects of the virus.
Article Abstract
Cell surface cortical actin is a regulatory target for viral infection. We aimed to investigate the effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on host cell cortical stiffness, an indicator of cortical actin structure. The receptor-binding domain (RBD) of SARS-CoV-2 Spike (S) protein induced a reduction in cortical stiffness in ACE2-expressing cells. The interaction of RBD with ACE2 caused the inactivation of Ezrin/Radixin/Moesin (ERM) proteins. We further investigated the effects of the RBD of SARS-CoV-2 Omicron variants, BA.1 and BA.5. These RBDs influenced cortical stiffness depending on their affinity for ACE2. Our study provides the first evidence that the interaction of the SARS-CoV-2 S protein with ACE2 induces mechanobiological signals and attenuates the cortical actin.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s13577-024-01142-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!