PMC:7408073 / 34079-35163 JSONTXT

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.

Inhibition of TMPRSS2 and ADAM17 metalloprotease activity. Inhibition of the serine protease TMPRSS2 (necessary for SARS-CoV-2 entry) by a clinically proven protease inhibitor has been recently suggested by Hoffmann and colleagues [13] and inhibition of ADAM17 enzymatic activity has been already proposed about ten years ago by Haga and colleagues [20]. Indeed, inhibition of ADAM17-mediated ACE2 shedding is expected to increase membrane ACE2 expression and therefore the probability of viral entry; nevertheless, in the early phases of the disease, inhibition of ACE2 circulating activity might be sufficient to inhibit the systemic RAS pathway upregulation and the development of severe forms of COVID-19. It is, in fact, possible that maintenance/recovery of correct organismal immune responses, by preventing ACE2-mediated immune suppression, in concert with cellular adaptive immune responses mediated by apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) systems [80] may anyway work to induce both an effective “immunization” and the viral eradication.