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Editorial
. 2020 Jul;40(7):1605-1607.
doi: 10.1161/ATVBAHA.120.314620. Epub 2020 Jun 24.

Platelets and Immunity: Going Viral

Milka Koupenova  1 , Jane E Freedman  1
Affiliations
Editorial

Platelets and Immunity: Going Viral

Milka Koupenova et al. Arterioscler Thromb Vasc Biol. 2020 Jul.
No abstract available

Keywords: COVID-19; Editorials; HIV; blood-borne pathogens; platelets; thrombosis.

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Figures

Figure 1:
Figure 1:. Activation of platelets by HIVpp and influenza and proposed activation of platelet-Toll like receptor 7 (TLR7) by SARS-CoV-2.
If SARS-CoV-2 (similarly to influenza or HIVpp) can be endocytosed by platelets, its degraded ssRNA would be first recognized by TLR7. Activation of TLR7 in a MyD88-IRAK-IKKb-SNAP23 dependent signaling would lead to P-selectin/CD40L surface expression and complement C3 release form α-granules. P-selectin and CD40L would mediate platelet-leukocyte interactions (predominantly neutrophils). C3 release would increase neutrophil-DNA release and ensures viral capture and removal. As viral infection progresses, C3-mediated netosis may be augmented by thrombin generated as a result of TF released from damaged tissue; thrombin will also directly increase thrombosis. During COVID19, TLR9, could also contribute to platelet activation and possible C3 release. TLR9 can be activated by mitochondrial-DNA and mitochondrial-DNA levels can be increased with tissue damage (or in the setting of obesity). Platelet-TLR9, similarly to TLR7, signals through the MyD88-IRAK-IKKb-SNAP23 pathway leading to granule release. It is not currently known if platelets can release C3 or netosis in a TLR9-dependent manner.
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