5 CONCLUSIONS
The evidence gathered in this study suggests that SARS-CoV-2 infection induces an oxidative response that potentiates cell damage evidenced by inhibition of mitochondrial function, morphological changes and cell death in leucocytes. The signaling associated with inflammation and oxidative stress in COVID-19 disease establishes a paradigm of comprehensive injury that must be consider in physiopathology. These processes explain the rapid changes in the immune system, and that present an initial over-activation and early massive death due to SARS-CoV-2 infection, promoting endothelial-alveolar damage that would cause multi-organ failure. From this, a relevant approach is shown to develop therapeutic strategies based on this and other early processes related to the pathogenic characteristics of the disease, although more research is needed to detail the mechanisms of cytotoxicity, it is essential to start establishing early actions in the therapy of this disease.
Acknowledgments: Thanks to MD. Rosa Elena Zamudio for provide the patient’s blood samples with COVID-19.