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Review
. 2020 Jul 26;13(8):166.
doi: 10.3390/ph13080166.

Immune Pathogenesis of COVID-19 Intoxication: Storm or Silence?

Mikhail Kiselevskiy  1 , Irina Shubina  1 , Irina Chikileva  1 , Suria Sitdikova  1 , Igor Samoylenko  1 , Natalia Anisimova  1 , Kirill Kirgizov  1 , Amina Suleimanova  1 , Tatyana Gorbunova  1 , Svetlana Varfolomeeva  1
Affiliations
Review

Immune Pathogenesis of COVID-19 Intoxication: Storm or Silence?

Mikhail Kiselevskiy et al. Pharmaceuticals (Basel). .

Abstract

Dysregulation of the immune system undoubtedly plays an important and, perhaps, determining role in the COVID-19 pathogenesis. While the main treatment of the COVID-19 intoxication is focused on neutralizing the excessive inflammatory response, it is worth considering an equally significant problem of the immunosuppressive conditions including immuno-paralysis, which lead to the secondary infection. Therefore, choosing a treatment strategy for the immune-mediated complications of coronavirus infection, one has to pass between Scylla and Charybdis, so that, in the fight against the "cytokine storm," it is vital not to miss the point of the immune silence that turns into immuno-paralysis.

Keywords: COVID-19; acute respiratory distress syndrome (ARDS); immuno-paralysis; lymphopenia; macrophage activation syndrome; “cytokine storm”.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Immunologic damage with COVID-19 infection. Pneumocytes infected with SARS-CoV-2 are recognized and lysed by innate (NK cells) and adaptive (T cells) immune effector cells. Activated lymphocytes produce a wide range of cytokines and phagocyte recruiting chemokines, which attract macrophages and neutrophils to the infection site. Activated macrophages and neutrophils release reactive oxygen species (ROS) that damage lung tissue. Macrophages are also induced via TLR7 interaction with viral RNA. Macrophage stimulation triggers pro-inflammatory cytokine overproduction and the “cytokine storm,” which results in systemic inflammatory response syndrome and multiple organ failure. Increased level of inflammation mediators leads to the apoptosis of immune effector cells, which causes lymphopenia and, subsequently, immunosuppression. Secondary bacterial infections may develop at this stage.
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