Extracellular Vesicle-Related Thrombosis in Viral Infection

Figures & data

Table 1 Population and Characteristics of EVs

	Exosome	MV (MP)	AB
Size	30–200 nm	100–1000 nm	1000–3000 nm
Shape	Homogeneous	Variable	Variable
Origine	MBV fusion with the plasma membrane	Budding from the plasma membrane	Budding from the plasma membrane
Markers	Tetraspanins (CD9, CD63, CD81) Alix, TSG101, HSP70	Annexin V, Integrin, Selectin, CD40 ligand, metalloproteinase	Annexin V, DNA fragment Caspase 3, Histones
Isolation	Ultracentrifugation (100,000g)	Ultracentrifugation (10,000–100,000g)	Ultracentrifugation (6000–10,000g)
P-Act	Weak	Powerful	Powerful

Notes: Data from Nomura.¹¹ All vesicles preparations are heterogeneous with different protocols allowing the enrichment of one type over another.

Abbreviations: MV, microvesicle; MP, microparticle; AB, apoptotic body; MBV, multivesicular body; TSG101, tumor susceptibility gene 101; HSP70, heat shock protein 70; P-Act, procoagulant activity.

Figure 1 Convergence of EV and virus biogenesis. Original cell owns the endocytic and secretory pathways. Viruses share effectors of EV production for their assembly and release. Exosomes produced in the MVB and shed MV (MP) budding of the plasma membrane. Apoptotic cell finally releases shedding AB.

Abbreviations: MV, microvesicle; MP, microparticle; AB, apoptotic body; N, nucleus; MBV, multivesicular body; ER, endoplasmic reticulum.

Figure 2 EV mediated thrombotic event pathway.

Abbreviations: EV, extracellular vesicle; MV, microvesicle; MP, microparticle; EC, endothelial cell; PAI-1, plasminogen activator inhibitor-1; VWF, von Willebrand factor.

Nomura S. Extracellular vesicles and blood diseases. Int J Hematol. 2017;105(4):392–405. doi:10.1007/s12185-017-2180-x28130731

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