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Abstract
Extracellular vesicles (EVs), which are cell released double layered membrane particles, have been found in every circulating body fluid, and provide a tool for conveying diverse information between cells, influencing both physiological and pathological conditions. Viruses can hijack the EVs secretory pathway to exit infected cells and use EVs endocytic routes to enter uninfected cells, suggesting that EVs and viruses can share common cell entry and biogenesis mechanisms. SARS-CoV-2 is responsible of the coronavirus disease 2019 (Covid-19), which may be accompanied by severe multi-organ manifestations. EVs may contribute to virus spreading via transfer of virus docking receptors such as CD9 and ACE2. Covid-19 is known to affect the renin angiotensin system (RAS), and could promote secretion of harmful EVs. In this scenario EVs might be linked to cardiovascular manifestations of the Covid-19 disease through unbalance in RAS. In contrast EVs derived from mesenchymal stem cells or cardiosphere derived cells, may promote cardiovascular function due to their beneficial effect on angiogenesis, fibrosis, contractility and immuno-modulation. In this article we assessed the potential impact of EVs in cardiovascular manifestations of Covid-19 and highlight potential strategies to control the extracellular signaling for future therapies.
Highlights
Cells are continuously secreting extracellular vesicles (EVs) that include large apoptotic bodies (1–5 μm), microvesicles (100–1,000 nm) or small exosomes (30–100 nm), which vary in their abundance, size, and composition
Post-mortem autopsy analysis showed that almost 35% of patients who succumbed to SARSCoV-1 presented detectable viral SARS-CoV-1 genome in heart samples, and this was associated with myocardial fibrosis, inflammation, and reduced myocardial angiotensin converting enzyme 2 (ACE2) expression (Oudit et al, 2009)
We have discussed the possible function of Extracellular vesicles (EVs) in Covid19 and highlight potential therapeutic application for EVs in modulating the virus infection, the pro-inflammatory state and cardiovascular disease in Covid-19
Summary
Cells are continuously secreting extracellular vesicles (EVs) that include large apoptotic bodies (1–5 μm), microvesicles (100–1,000 nm) or small exosomes (30–100 nm), which vary in their abundance, size, and composition. It might be possible that SARS-CoV-2 infected cells increase the production of exosomes enriched in viral components In this way, exosomes containing pathogenic proteins and RNA released from infected cells may induce host humoral and cellular immune response (Gunasekaran et al, 2017) and could potentially play anti-infective roles (Zhang et al, 2018). SARS-CoV-2 viral particles have been found in cardiac biopsies of Covid-19 patients (Dolhnikoff et al, 2020; Tavazzi et al, 2020), and it has been reported that this virus can infect human cardiomyocytes and induce cardiotoxicity (Bojkova et al, 2020) Both SARS-CoV-1 and SARS-CoV-2 uses ACE2 as docking station to infect target cells and the internalization of virus/enzyme complex leads to loss of enzymatically active ACE2 at the cell surface (Gheblawi et al, 2020; Hoffmann et al, 2020). The antiinflammatory activity of EVs indicate that this platform can work well in xenogenic applications (de Couto et al, 2017; Gallet et al, 2017), which could simplify the large scale production of EVs for therapeutic applications by using MSCs or CDC derived from large animals rather than humans
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