As it is already known so far, the COVID-19-associated incidence and mortality are explained by pathological changes of an immune response of the patient. Two contradictory hypotheses are made: the defeat mediated by a hyper inflammatory "tsitokinovy storm" and the disturbance of an immunologic protective mechanism of the owner leading to uncontrollable spread of a virus and defeat of bodies. The lack of diagnostic tools for assessment of immune function is the key reason of inability to explain such contradiction at COVID-19 infection.
One of the most remarkable facts about the current epidemic of SARS-CoV-2 (COVID-19) is that, despite the researches which are actively conducted worldwide, pathophysiological processes playing a crucial role in incidence and mortality among patients still remain unknown. The paradigm of pathological process dominating now means that too strong immune response as which mediators excessively produced pro-inflammatory cytokines act causes extensive damage of lungs and a condition of tendency to fibrinferments. Respectively, it is supposed that the lethal outcome comes first of all because of an inflammatory disease of lungs, disturbance micro and macrocirculation and the respiratory insufficiency or a vascular coagulopathy coming finally. This concept of the lethal outcome mediated by "a tsitokinovy storm" among patients with COVID-19 is spread both in unspecialized printing editions, and in many leading scientific publications.
On the basis of the above theory tests of a number of antitsitokinovy and antiinflammatory therapies for treatment of COVID-19, including antibodies to interleukin-6, antagonists of a receptor of interleukin-1 and inhibitors of an alarm way JAK-STAT are carried out, but during earlier clinical trials the essential efficiency of such approaches did not manage to be proved.
At the same time, as it is paradoxical, the second, opposite theory of the COVID-19-induced incidence and mortality consists in collapse of a system of immunity of the patient. Such collapse of immunity is shown in inability to constrain its uncontrollable replication and spread of a virus along with direct cytotoxicity of products of an immune response of the patient. The progressive and deep lymphopenia observed at patients which levels sometimes reach the same values, as is given as justification of this opposite theory at AIDS. Results of many recently executed researches demonstrate that, unlike "a tsitokinovy storm" which often is considered incidental the lymphopenia remains at critically sick patients with COVID-19 and correlates with the increased weight of secondary diseases and a lethal outcome.
The personalized approach to delivery of health care demands fuller understanding, reaction of a system of immunity, what of these types, prevails as suitable interventions will differ radically depending on diagnosis — existence at the patient of hyperreactivity or deep immunosuppression. For example, clinical trial of antibodies against interleukin-6 is carried out now, antagonists of a receptor of IL-1 and JAK-STAT inhibitors as therapeutic means for treatment of patients with COVID-19 and there is a probability that they can break even more ability of an organism of the patient to overcome a virus. On the other hand, therapy methods with use of immunostimulators, for example, of inhibitors of immune control points of interleukin-7, интерферона-γ or GM-CSF, can aggravate the violated and steady inflammatory answer and lead to strengthening of extent of defeat of bodies.
Summarizing the aforesaid, becomes clear that when maintaining critically sick patients with COVID-19 it is necessary to answer two concrete and being key a question:
1) what their primary immune endotype i.e. whether it is hyperreactive or immunosuppressive;
2) how this state changes in connection with progressing of a disease or normalization of a state eventually.
Fuller understanding of the immune status of the patient with COVID-19 will help to carry out the correct immunotherapy. Definition will be a problem of the subsequent researches in this area whether develops at COVID-19 the strengthened pro-inflammatory "tsitokinovy storm" or the state developing at the specified pathology represents immunosuppressive type of an immune response and also studying as function of the immune system in process of progressing of a disease changes.