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Updated: Jul 13, 2025
Author Spotlight: A Pseudotype Virus System for Assessing Omicron Subvariants and Neutralizing Antibodies in SARS-CoV-2 Research
Published on: September 8, 2023
SARS-CoV-2 Omicron variant infection affects blood platelets, a comparative analysis with Delta variant
Cédric Garcia1,2, Baptiste Compagnon1,3, Agnès Ribes1,2
1Inserm UMR1297 and Université Toulouse 3, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Toulouse, France.
Introduction:
In November 2021, the SARS-CoV-2 Omicron variant of concern has emerged and is currently dominating the COVID-19 pandemic over the world. Omicron displays a number of mutations, particularly in the spike protein, leading to specific characteristics including a higher potential for transmission. Although Omicron has caused a significant number of deaths worldwide, it generally induces less severe clinical signs compared to earlier variants. As its impact on blood platelets remains unknown, we investigated platelet behavior in severe patients infected with Omicron in comparison to Delta.
Methods:
Clinical and biological characteristics of severe COVID-19 patients infected with the Omicron (n=9) or Delta (n=11) variants were analyzed. Using complementary methods such as flow cytometry, confocal imaging and electron microscopy, we examined platelet activation, responsiveness and phenotype, presence of virus in platelets and induction of selective autophagy. We also explored the direct effect of spike proteins from the Omicron or Delta variants on healthy platelet signaling.
Results:
Severe Omicron variant infection resulted in platelet activation and partial desensitization, presence of the virus in platelets and selective autophagy response. The intraplatelet processing of Omicron viral cargo was different from Delta as evidenced by the distribution of spike protein-positive structures near the plasma membrane and the colocalization of spike and Rab7. Moreover, spike proteins from the Omicron or Delta variants alone activated signaling pathways in healthy platelets including phosphorylation of AKT, p38MAPK, LIMK and SPL76 with different kinetics.
Discussion:
Although SARS-CoV-2 Omicron has different biological characteristics compared to prior variants, it leads to platelet activation and desensitization as previously observed with the Delta variant. Omicron is also found in platelets from severe patients where it induces selective autophagy, but the mechanisms of intraplatelet processing of Omicron cargo, as part of the innate response, differs from Delta, suggesting that mutations on spike protein modify virus to platelet interactions.
Insights
The Omicron variant activates and desensitizes blood platelets, similar to the Delta variant. However, Omicron
Area of Science:
- Hematology
- Virology
- Immunology
Background:
- The emergence of the SARS-CoV-2 Omicron variant in November 2021 has led to global dominance of the COVID-19 pandemic.
- Omicron exhibits numerous spike protein mutations, contributing to increased transmissibility and distinct clinical characteristics compared to previous variants.
- While generally causing less severe disease, Omicron's specific impact on blood platelets remains largely uncharacterized.
Purpose of the Study:
- To investigate and compare platelet behavior in severe COVID-19 patients infected with the Omicron variant versus the Delta variant.
- To analyze platelet activation, responsiveness, phenotype, and viral presence within platelets.
- To explore the direct effects of Omicron and Delta spike proteins on healthy platelet signaling pathways.
Main Methods:
- Analysis of clinical and biological data from severe COVID-19 patients infected with Omicron (n=9) or Delta (n=11).
- Utilized flow cytometry, confocal imaging, and electron microscopy to assess platelet characteristics and viral interactions.
- Investigated the direct impact of isolated Omicron and Delta spike proteins on healthy platelet signaling.
Main Results:
- Severe Omicron infection induced platelet activation, partial desensitization, and selective autophagy, with the virus detected within platelets.
- Intraplatelet processing of Omicron viral components differed from Delta, evidenced by spike protein distribution and Rab7 colocalization.
- Both Omicron and Delta spike proteins activated signaling pathways in healthy platelets, including AKT, p38MAPK, LIMK, and SPL76 phosphorylation, with distinct kinetics.
Conclusions:
- Despite differing biological characteristics, Omicron, like Delta, causes platelet activation and desensitization in severe COVID-19.
- The virus is present in platelets, triggering an innate selective autophagy response, but with altered intraplatelet processing mechanisms compared to Delta.
- Mutations in the Omicron spike protein appear to modify virus-platelet interactions, influencing the innate immune response.
