TP53 Dysregulation during SARS-CoV-2 Infection: Molecular Mechanisms, Cellular Consequences, and Therapeutic Perspectives
DOI:
https://doi.org/10.46966/msjar.v7i2.416Keywords:
COVID-19; SARS-CoV-2; TP53; p53; MDM2; DNA Damage; Apoptosis; Cancer Biology; Long COVIDAbstract
Background: Overview of COVID-19 pathogenesis and the central role of TP53 in maintaining genomic stability, DNA repair, apoptosis, immune regulation, and tumor suppression. Objective: To summarize current evidence regarding the interaction between SARS-CoV-2 infection and the TP53 signaling pathway and discuss potential cellular and clinical consequences. Methods: A literature search was performed using PubMed, Scopus, Web of Science, and Google Scholar for studies published between 2020 and 2026. Results: Emerging evidence indicates that SARS-CoV-2 may suppress p53 activity through multiple molecular mechanisms involving MDM2-mediated degradation, modulation of antiviral signaling pathways, and interference with cellular stress responses. Reduced p53 activity may contribute to enhanced viral replication, impaired DNA repair, altered apoptosis, excessive inflammation, and immune dysregulation. Conclusion: Although current evidence supports transient dysregulation of TP53 signaling during SARS-CoV-2 infection, additional clinical and longitudinal studies are required to determine whether these alterations contribute to long-term pathological consequences, including carcinogenesis.
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Copyright (c) 2026 Ali Ayad Abd Al-Hassan, Abdulrahman Salim Qatia Alazzamee, Haneen Ali Darsoon Alshabbani
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