Is #SARS-CoV-2 an #oncogenic #virus? - #JournalofInfection https://t.co/vaJVAEqUP7 #AlbertoGómezCarballa#FedericoMartinónTorres#AntonioSalas#GENVIP, Instituto de Investigación Sanitaria de Santiago, #Universidade de #SantiagodeCompostela, Santiago de Compostela, #Spain
— Guillermo Ruiz Zapatero (@ruiz_zapatero) October 31, 2022
Recently, in this journal, Wu et al. (1) and Gao et al. (2) have both indicated that host genetic variation related to COVID-19 might be associated to endometrial cancer. We here add evidence from gene expression analysis supporting that the connection of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and cancer could be more general, in line with several other viral infections that represent serious risks for carcinogenesis in humans. The SARS-CoV-2 has developed similar strategies to Epstein-Barr virus (EBV) and hepatitis B virus (HSV1) to control p53 by hijacking the protein via virus antigens, and ultimately leading to its degradation (3,4). Specifically, the Nsp2 viral protein of the SARS-CoV-2 interacts with the prohibitin 1 and 2 (PHB1, PHB2) that are primarily located in the mitochondrion and play an essential role in maintaining mitochondrial DNA activity. Their depletion triggers a chain of cell responses that lead to a leakage of reactive oxygen species (ROS) to the nucleus and oxidative damage, that ultimately provokes the impairment of the transactivation of p53-dependent genes. In addition, the Nsp3 SARS-CoV-2 protein binds and activates the RING finger and CHY zinc finger domain-cotainin protein 1 (RCHY1) and E3 ubiquitin ligase, promoting p53 degradation (5). Therefore, SARS-CoV-2 has the ability to trigger external and internal apoptotic pathways of the host cells, facilitating its spread. Impairment of p53 could be seen as a strategy of the virus to take advantage of the cell pathways controlled by this protein for its own benefit during acute phase of infection, therefore evading host immune response and facilitating its replication (3). In this context, a reduced expression of p53 during the acute phase of infection is also a biomarker of severe disease.
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