Publication date: Sep 22, 2023

COVID-19 disease is associated with an increased risk of thrombotic complications, which contribute to high short-term mortality. Patients with COVID-19 demonstrate enhanced platelet turnover and reactivity, which may have a role in the development of thrombotic events and disease severity. Evidence has suggested direct interaction between SARS-CoV-2 and platelets, resulting in platelets activation. Here, we compare the effect of various SARS-CoV-2 spike variants on platelet activation. Engineered lentiviral particles were pseudotyped with spike SARS-CoV-2 variants and incubated with Platelet Rich Plasma obtained from healthy individuals. The pseudotyped SARS-CoV-2 exhibiting the wild-type Wuhan-Hu spike protein stimulated platelets to increase expression of the surface CD62P and activated αIIbβ3 markers by 3. 5 +/- 1. 2 and 3. 3 +/- 0. 7 fold, respectively (P = 0. 004 and 0. 003). The Delta variant induced much higher levels of platelet activation; CD62P expression was increased by 6. 6 +/- 2. 2 fold and activated αIIbβ3 expression was increased by 5. 0 +/- 1. 5 fold (P = 0. 005 and 0. 026, respectively). The Omicron BA. 1 and the Alpha variants induced the lowest level of activation; CD62P expression was increased by 1. 7 +/- 0. 4 and 1. 6 +/- 0. 9 fold, respectively (P = 0. 003 and 0. 008), and activated αIIbβ3 expression by 1. 8 +/- 1. 1 and 1. 6 +/- 0. 8, respectively (P = 0. 003 and 0. 001). The Omicron BA. 2 variant induced an increase of platelets activation comparable to the Wuhan-Hu (2. 8 +/- 1. 2 and 2. 1 +/- 1. 3 fold for CD62P and activated αIIbβ3 markers, respectively). The results obtained for various COVID-19 variants are in correlation with the clinical severity and mortality reported for these variants.

Semantics

Original Article