Development and standardization of experimental models of SARS-CoV-2 virus infection

COVID-19, the disease caused by the SARS-CoV-2 virus, is a major cause of public health concern worldwide. Scientists in basic and clinical areas around the world are having significant effects on the understanding of the pathophysiology and the investigation or effect of drugs with antiviral action and the repositioning of drugs that perform anti-inflammatory action, and there is still no medicine or clinical treatment for patients a COVID-19. However, it is known that progressive respiratory failure causes damage caused by alveolar cells, is caused by viral replication, and excessive local inflammation, is one of the major obstacles to the recovery of critically ill patients with COVID-19. In this sense, the host's defense against infections depends not only on the mechanisms of immune resistance but also on the organism's ability to tolerate the damage that a determined individual promotes. An amphiregulin (AREG) is a central factor that promotes repair and restoration of tissue integrity after tissue damage associated with inflammation. AREG-deficient animals have a substantial impairment of the ability to restore lung function in infection models. In addition, the administration of recombinant AREG enhances the tissue repair process after tissue damage resulting from excessive inflation. Our working hypothesis is that AREG plays a crucial role in repairing and restoring the integrity of lung tissue during a COVID-19 and that treatment with AREG is recombinant during the patients' recovery period. Thus, we propose in the present project to standardize the experimental model of Sars-CoV-2 infection and to investigate the role of AREG in the pathophysiology of COVID-19