PARADIGMS OF COVID-19 AND THE CYTOKINE THERAPY APPROACHES

Abstract

One of the complications caused by the viral agent SARS-CoV2 is atypical pneumonia that occurs classically in viral pathologies. These infection complications produce a sort of “cytokine release syndrome” that sees interleukin 6, a glycosylated protein of approximately 212 amino acids, among the leading players in the inflammatory process. IL-6 typically produces a transient inflammatory state that promotes the host’s immune defence through its pleiotropic function. There is the stimulation of a response in the acute infectious phase, hematopoiesis and the regular advent of immune reactions. The action of the anti-inflammatory cytokines, which tends to regulate the inflammatory one’s activity, is directed to the same cells that produce IL-6, which, through an inhibition mechanism, slow down or production ceases altogether. Evidently, in the case of the IL-6 storm, the action of these anti-inflammatory cytokines is insufficient, and the blockade of IL-6R receptors and through the use of monoclonal antibody-like tocilizumab has proved to be optimal to manage complications and avoid potentially fatal situations. Therefore, the purpose of this paper is to create a mathematical model that describes the action of the IL-6 cytokine in SARS-CoV2 virus infection to understand better the extent of the disease itself and the associated severe side effects. We represent the concentration of tocilizumab, soluble IL-6R, absolute neutrophils and circulating platelets using computational modeling. Tocilizumab is administered by intravenous infusions with a minimum dose of 80[Formula: see text]mg and a maximum dose of 400[Formula: see text]mg. Following tocilizumab administration, simulation results indicate that the population of absolute neutrophils and circulating platelets is decreasing. After the removal of tocilizumab concentration, both absolute neutrophils and circulating platelets return at their baselines.