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Respiratory viral infections such as SARS-CoV-2 affect immune homeostasis by altering the immune regulatory network leading to decreased responsiveness, changes in lymphocyte sub-populations and decreased macrophage function1 . Clinically, the immune response induced by SARS-CoV-2 infection occurs in two phases: the first immune defence-based protective phase and the second inflammation-driven damaging phase2 . The first immune defence-based protective phase is characterized by recruitment of antibody-secreting cells, follicular helper T-cells, activated CD4 and CD8 T-cells and immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies that bind to SARS-CoV-2 (ref.3). The second phase leads to uncontrolled cytokine release causing cytokine release syndrome (CRS), or ‘cytokine storm’ characterized by increased IL-2, IL-7, granulocyte colony stimulating factor, IFN-gamma and TNF-alpha4 . CRS damages tissues of the lungs, kidney and heart leading to rapid multiorgan failure. The deaths from COVID-19 are due to massive alveolar damage leading to acute respiratory distress syndrome (ARDS) that culminates in respiratory failure. Restoration of Th1/Th-2 cytokine balance is one of the mechanisms of establishing immune homeostasis5,6 .
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