SARS-CoV-2 is all able to control cellular pathways, remodeling their ability to contrast viral infection. The peculiar ability of SARS-CoV-2 to degrade p53 leads to decreased cell apoptosis favoring viral growth in infected cells as well as to the loss of the antiviral activity of p53. In this regard, p53 is a pleiotropic molecule related to antiviral innate immune responses carried out particularly by inducing apoptosis of infected cells and mediating type I interferon (IFN) production/signaling. In the context of antiviral immunity, p53 plays therefore a critical role and perhaps this is why it represents a frequent viral target. The inhibition of virus-target cells apoptosis exacerbates inflammation increasing the levels of key inflammatory mediators, referred as “cytokine storm”.
A potential new therapeutic approach might be Idasanutlin, a second-generation potent and selective small-molecule MDM2 antagonist with a pyrrolidine structure. Idasanutlin shows an identical cellular mechanism to other Nutlin family molecules, but with an enhanced potency, selectivity, and bioavailability as non-genotoxic activators of p53.
The current pharmacological approaches to control SARS-CoV-2 infection are mainly aimed to interfere with binding and entry of viruses into human cells, to interfere with the translation and proteolysis of the polyprotein complex, to interfere with the replication of viral RNA, to inhibit viral release. Emerging clinical data has revealed that severe COVID-19 disease is associated with heightened inflammatory responses, suggesting that patient treatment strategies must extend beyond antiviral agents. This Research Topic aims to explore and cover the current knowledge and research trends of pharmacological treatment for COVID-19 patients not targeted against SAS-CoV-2 but on cell cycle control to contrast SARS-CoV-2 infection and to modulate host immunity and inflammatory responses.
We welcome the submission of Original Research, Reviews, Mini Reviews, Methods, Case Reports, and Perspective articles focused on the different aspects of the role of cell cycle control and SARS-CoV-2 infection which include but are not limited to:
1) In vitro and in vivo basic research as well as clinical reports on the role of cell cycle control drugs in SARS-CoV-2 infection;
2) Innovative methodologies to study cell cycle control drugs in SARS-CoV-2 infection, especially, but not limited to, the central nervous system;
3) Potential therapeutical approaches based on the control of SARS-CoV-2 infection via cell cycle control.
SARS-CoV-2 is all able to control cellular pathways, remodeling their ability to contrast viral infection. The peculiar ability of SARS-CoV-2 to degrade p53 leads to decreased cell apoptosis favoring viral growth in infected cells as well as to the loss of the antiviral activity of p53. In this regard, p53 is a pleiotropic molecule related to antiviral innate immune responses carried out particularly by inducing apoptosis of infected cells and mediating type I interferon (IFN) production/signaling. In the context of antiviral immunity, p53 plays therefore a critical role and perhaps this is why it represents a frequent viral target. The inhibition of virus-target cells apoptosis exacerbates inflammation increasing the levels of key inflammatory mediators, referred as “cytokine storm”.
A potential new therapeutic approach might be Idasanutlin, a second-generation potent and selective small-molecule MDM2 antagonist with a pyrrolidine structure. Idasanutlin shows an identical cellular mechanism to other Nutlin family molecules, but with an enhanced potency, selectivity, and bioavailability as non-genotoxic activators of p53.
The current pharmacological approaches to control SARS-CoV-2 infection are mainly aimed to interfere with binding and entry of viruses into human cells, to interfere with the translation and proteolysis of the polyprotein complex, to interfere with the replication of viral RNA, to inhibit viral release. Emerging clinical data has revealed that severe COVID-19 disease is associated with heightened inflammatory responses, suggesting that patient treatment strategies must extend beyond antiviral agents. This Research Topic aims to explore and cover the current knowledge and research trends of pharmacological treatment for COVID-19 patients not targeted against SAS-CoV-2 but on cell cycle control to contrast SARS-CoV-2 infection and to modulate host immunity and inflammatory responses.
We welcome the submission of Original Research, Reviews, Mini Reviews, Methods, Case Reports, and Perspective articles focused on the different aspects of the role of cell cycle control and SARS-CoV-2 infection which include but are not limited to:
1) In vitro and in vivo basic research as well as clinical reports on the role of cell cycle control drugs in SARS-CoV-2 infection;
2) Innovative methodologies to study cell cycle control drugs in SARS-CoV-2 infection, especially, but not limited to, the central nervous system;
3) Potential therapeutical approaches based on the control of SARS-CoV-2 infection via cell cycle control.
