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SARS-CoV-2 immune complex triggers human monocyte necroptosis
Leonardo Duarte Santos1, Krist Helen Antunes1, Gisele Cassão1
1Laboratory of Clinical and Experimental Immunology, Infant Center, School of Life and Health Science, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Brazil.
International Immunopharmacology
|March 4, 2023
Summary
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) triggers necroptosis, a form of cell death, in human monocytes. This process involves specific proteins and may contribute to COVID-19 pathogenesis.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is associated with significant morbidity and mortality.
- Understanding the mechanisms of viral-induced cell death is crucial for developing effective treatments.
- Monocytes play a key role in the innate immune response to viral infections.
Purpose of the Study:
- To investigate the role of necroptosis in SARS-CoV-2 infection.
- To determine whether SARS-CoV-2 and its immune complexes can induce necroptosis in human monocytes.
- To elucidate the molecular pathways involved in SARS-CoV-2-induced necroptosis.
Main Methods:
- Analysis of monocyte necroptosis induction by SARS-CoV-2 and SARS-CoV-2-IgG immune complexes.
- Assessment of the involvement of necroptosis-associated proteins (RIPK1, RIPK3, MLKL) and Syk tyrosine kinase.
- Measurement of lactate dehydrogenase (LDH) levels as a marker of cell death.
Main Results:
- SARS-CoV-2 induced MLKL-dependent necroptosis in monocytes.
- Necroptosis-associated proteins were involved in SARS-CoV-2 N1 gene expression.
- SARS-CoV-2 immune complexes induced necroptosis via Fcγ receptors, requiring RIPK3, MLKL, and Syk kinase.
- Elevated LDH levels correlated with COVID-19 pathogenesis.
Conclusions:
- SARS-CoV-2 directly induces necroptosis in human monocytes.
- SARS-CoV-2 immune complexes exacerbate necroptosis through Fcγ receptor signaling.
- Necroptosis and elevated LDH levels are implicated in the pathogenesis of COVID-19.
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