Editorial: Cell cycle control as a new therapeutic approach for SARS-CoV-2 infection

SARS-CoV-2 can manipulate cellular pathways, changing how well they can resist viral infection. Because of SARS-CoV-2 capacity to destroy p53, less cell death occurs in infected cells, which promotes viral replication, and p53 antiviral action is lost. Regarding this, p53 is a pleiotropic molecule associated with antiviral innate immune responses, which are specifically carried out by triggering apoptosis of infected cells and facilitating type I interferon (IFN) production/signaling. p53 consequently plays a crucial role in the setting of antiviral immunity, which may be why it is frequently targeted by viruses. By preventing virus-targeted cells from undergoing apoptosis, inflammation is made worse and a “cytokine storm” is produced. The major goals of the current pharmacological techniques to control SARS-CoV2 infection are to prevent viral binding and entry into human cells, to obstruct polyprotein complex translation and proteolysis, to obstruct viral RNA replication, and to limit viral release. The severity of COVID-19 disease is linked to heightened inflammatory responses, according to newly available clinical data, indicating that patient treatment plans should go beyond antiviral drugs.