Study of a Possible Respiratory Degradation Prognosis Caused by Biomarkers in Severe Forms of COVID-19 Pneumonia

Overview

Respiratory infection with the SARS-CoV2 virus is associated with a major risk of viral pneumonia that can lead to respiratory distress requiring resuscitation. In the most severe forms, it may require a mechanical ventilation or even lead to an acute respiratory distress syndrome with a particularly poor prognosis. The SARS-CoV2 is a single-stranded RNA virus of positive polarity and belongs to the beta genus of Coronaviruses. SARS-CoV2 is responsible for the third epidemic in less than twenty years secondary to a Coronavirus (SARS-CoV then MERS-CoV) and if the mortality associated with it is lower than that of previous strains, particularly MERS-CoV (Middle East Respiratory Syndrome), its spread is considerably bigger. As a result, the number of patients developing respiratory distress that require an invasive mechanical ventilation is high, with prolonged ventilation duration in these situations.

The mechanisms responsible for alveolar damage during viral pathologies, particularly Coronavirus, are very similar to those observed during acute respiratory distress syndromes in adults. Macrophages present in the pulmonary parenchyma appear to play a central role in the severity of the inflammatory response and the production of proinflammatory mediators, notably chemokines leading to secondary leukocyte infiltration. The recent monocytic origin could explain the particular severity of this inflammatory response whose usual control is no longer assured. The alteration of infectious control by alveolar macrophages during ageing also tends to confirm the central role of these cells in the pattern of respiratory distress observed during COVID-19 infection, which is particularly severe in the elderly. In many situations, the endotoxin (or lipopolysaccharide, LPS) plays a major role in the pathophysiology and even the severity of respiratory damage, in particular, due to the existence of circulating endotoxin from the pathogenic agent responsible (Gram-negative bacteria), but also due to translocation of digestive origin in the context of sepsis (systemic inflammatory response) which is associated with (if not responsible for) respiratory aggression. Such an alteration of the mucous membrane is particularly noticeable in cases of obesity. The importance of this mechanism during pulmonary aggression of viral origin is, on the other hand, unknown. Few data are available on the prediction of early onset of respiratory distress syndrome in low respiratory infection in the absence of mechanical ventilation.