Immunopathogenesis of the progress of the seriously ill patient with COVID-19

Abstract

Background: around five percent of the patients with COVID-19 have a critical progress, with respiratory failure, and approximately half of them die; the competence of the patient immune system is invoked as a factor that defines this progress.

Objective: to describe immunopathogenesis in the progress of the seriously ill patient with COVID-19.

Methods: a review was carried out in: PubMed, Sciencdirect, the SciELO network, in addition to using the Google Academic search engine. Combinations of terms were used, such as: COVID-19, immune system, lymphopenia, cytokinemia, comorbidities and critically ill patient.

Results: the subject is being treated with intensity in the scientific literature, with a predominance of theories that still require a greater amount of evidence. In general, it is established that: a non-competent immune system, with an imbalance in the response of cooperating T lymphocytes, derives the anti-viral response with a predominance of an inflammatory response (Th17), rather than to cellular immunity (Th1), a mechanism par excellence in the elimination of intracellular pathogenic microorganisms; proinflammatory hypercytokinemia, the activation of biological alternatives that amplify the inflammatory response such as the coagulation cascade, generate more tissue damage and promote thrombotic phenomena that, together with lymphopenia, characterize the process with a greater clinical severity. Patients with endothelial dysfunction due to immunosenescence and comorbidities are at risk for this progress.

Conclusions: the pathogenesis is multifactorial, where a predisposing genetic basis, the triggering viral infection and the imbalance as an aggravating factor, are responsible for the multiple pathogenic mechanisms described up to now.