Immune dysregulation in coronavirus infection COVID-19

Immune dysregulation is one of the main causes of severe coronavirus infection COVID-19. The immune response in COVID-19 is characterized by the activation of innate immune cells and elevated levels of pro-inflammatory cytokines in the blood (tumor necrosis factor alpha, interleukins-1, -6, -8), neutrophils, C-reactive protein and ferritin. Organ dysfunction, including acute respiratory distress syndrome, is associated with cytokine storm. Another important sign of immune dysregulation is lymphopenia, one of the key predictor of the development of severe COVID-19 and poor outcome. One of the main causes of lymphopenia in patients with severe COVID-19 is apoptosis of lymphocytes. The increased proinflammatory cytokines play a critical role in the induction of lymphocytes apoptosis and lymphopenia. The clinical role of lymphocytes apoptosis in COVID-19 is associated with the immunosupression and the opportunistic and secondary infectious diseases. The immunosupression in severe COVID-19 is confirmed by the results of morphological studies demonstrating the depletion of lymphocytes in lymphoid tissue. Next important cause of lymphopenia is lymphocyte sequestration in the lungs. Postmortem studies of the lungs of patients died from COVID-19 show the lymphocytic infiltration. Additionally, lymphopenia may result from impaired lymphopoiesis due to virus-induced damage to lymphocyte precursors in the bone marrow and thymus. In COVID-19 patients, there is a significant reduction in the production of T-cells in the thymus. The decreased thymic function may exacerbate lymphopenia in patients during the acute phase of COVID-19 and prolong the time required for the recovery of circulating T-cell counts.