Abstract
The COVID-19 pandemic is a global challenge, demanding researchers address different approaches in relation to prevention, diagnostics and therapeutics. Amongst the many tactics of tackling these therapeutic challenges, small extracellular vesicles (sEVs) or exosomes are emerging as a new frontier in the field of ameliorating viral infections. Exosomes are part of extracellular vesicles (EVs)—spherical biological structures with a lipid bilayer of a diameter of up to 5000 nm, which are released into the intercellular space by most types of eukaryotic cells, both in physiological and pathological states. EVs share structural similarities to viruses, such as small size, common mechanisms of biogenesis and mechanisms for cell entry. The role of EVs in promoting the viral spread by evading the immune response of the host, which is exhibited by retroviruses, indicates the potential for further investigation and possible manipulation of these processes when tackling the spread and treatment of COVID-19. The following paper introduces the topic of the use of exosomes in the treatment of viral infections, and presents the future prospects for the use of these EVs.
Highlights
As scientists have yet to come to a consensus on specific markers that would clearly distinguish, for example, exosomes from ectosomes, the authors of MISEV2018 strongly encourage the use of the general term “EVs” to describe all extracellular vesicles [34]
The term “exosome” is defined as a small (< 200 nm) extracellular vesicle released on exocytosis of multi-vesicular bodies (MVBs) filled with intraluminal vesicles (ILVs) [34,37]
Extracellular vesicles are spherical biological structures with a lipid bilayer of a diameter of up to 5000 nm, which are released into the intercellular space by most types of eukaryotic cells, both in physiological and pathological states [34,35,36,37,38,39]
Summary
Exosomes were first described in 1981, as fragments of the membrane isolated from the biofluid [24]. Several different mechanisms for MVB formation, vesicle release and vesicle sorting have been proposed, the best known is the endosomal sorting complex required for transport (ESCRT). The ceramide and PA generated in this way on the MVB limiting membrane form a conical structure that may contribute to the negative curvature of the endosomal membrane [57,58] The result of this process is inward budding and the final formation of ILVs. The transport of MVB to the cell membrane is mainly driven by the Rab family of small GTPase proteins. The topology of EVs (including exosomes) indicates that their fusion with the cytosol or endosome membranes in the cell would require specific machinery that would differ from the SNARE proteins used for intracellular vesicle fusion [78].
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