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.