The infection by the SARS-CoV-2 can cause acute respiratory distress and can even lead to death in some patients. Although we know that COVID-19 is associated with excessive inflammation, the pathophysiological background has not been elucidated. Theodora Psaltopoulou, Yannis Danasis, Panos Malandrakis and Thanos Dimopoulos (Dean of the National and Kapodistrian University of Athens) summarize the findings of the study by Caroline Junqueira and colleagues recently published in the prestigious journal Nature (Junqueira, C. et al. FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation. Nature (2022)).
The monocytes and macrophages are at the forefront of the body's defence against infection. Recognition of the invasion of the infectious agent into the body by these cells leads to the generation of the inflammatory particle that activates caspase-1 and gastramine D, which then leads to inflammatory cell death (pyroptosis) and release of potent inflammation mediator molecules.
In this study the investigators showed that about 6% of monocytes in the peripheral blood of patients with COVID-19 are infected with SARS-CoV-2 virus. The infection of monocytes depends on the binding of the opsonized virus with antibodies to the Fcγ receptors of the monocytes. It is worth noting that the presence of antibodies against SARS-CoV-2 following vaccination against COVID-19 is not associated with an increased probability of monocyte infection by the virus in case of SARS-CoV-2 infection.
Once the virus enters the cells, it begins to multiply within them. However, the course of the infection and further spread of the virus into healthy cells is halted. The infected cells are then driven to inflammatory cell death (pyroptosis) through activation of the inflammatory bodies NLRP3 and AIM2, and the signaling pathway of caspase-1 and gastramine D. In addition, research data from lungs of patients who have terminated due to COVID-19 show that tissue macrophages have activated inflammatory bodies. However, no inflammatory bodies are observed in epithelial and endothelial cells infected by SARS-CoV-2.
In conclusion, the results of this study suggest that antibody-mediated endocytosis of SARS-CoV-2 virus by monocytes and macrophages triggers inflammatory cell death. On the one hand, this stops viral replication and further cell infection. On the other hand, however, potent (pro)inflammatory factors are activated that contribute to the pathogenesis of COVID-19.
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