Abstract
In response to the present coronavirus disease 2019 (COVID-19) pandemic, it is important to understand the infection pathogenesis of SARS-CoV-2. Sputum samples from 20 COVID-19 patients and healthy controls were collected, respectively. During the isolation of infectious SARS-CoV-2 virus, exosome-like vesicles were found associated with virions under transmission electron microscope. Next, the expression of IL6 and TGF-β increased in exosomes derived from the sputum of patients, and these were highly correlated with the expression of the SARS-CoV-2 N protein. Further, proximity barcoding assay (PBA) was used to investigate the immune related proteins in the exosomes, as well as the relationship between exosomes and SARS-CoV-2 N protein in COVID-19 patients’ samples. Particularly, to investigate the differential contribution of the specific exosome subsets, the protein expression of a single exosome was detected and analyzed for the first time. Among the 40 exosome subpopulations, 18 were found to have significant differences. The exosome subpopulation regulated by CD81 were most likely to correlate with the changes in the pulmonary microenvironment after SARS-CoV-2 infection. This study provides evidence on the association between exosomes and SARS-CoV-2 virus and promotes our understanding on possible pathogenesis of SARS-CoV-2 infection.Funding Statement: This work is supported by the emergency grants for prevention and control of SARS-CoV-2 of Ministry of Guangdong province (2020B111133001), the China Postdoctoral Science Project (2020T130025ZX and 2019M652860), the National Key Research and Development Program of China (2016YFC1304101), the Independent project of the State Key Laboratory of Respiratory Diseases (SKLRD-QN-201913), and the Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program (2017BT01S155).Declaration of Interests: The authors have declared that no conflict of interest exists.Ethics Approval Statement: The present study obtained the approval of the Ethics Committee of the First Affiliated Hospital of Guangzhou Medical University (Guangzhou, China).
Highlights
There are more than 179.27 million confirmed coronavirus disease 2019(COVID-19) cases, with more than 5,089,384 deaths reported to WorldOmeters as of Nov. 11, 2021
Twelve of the 20 COVID-19 required ventilator, who was diagnosed with acute respiratory distress syndrome (ARDS)
The protein matrix of cluster 4 shows that the expression of CD81 is the most and abnormally high (Figure 6D). These results suggest that the Extracellular vesicles (EV) regulated by CD81 are the most likely subpopulations of EVs that cause the changes in the pulmonary microenvironment after SARS-CoV-2 infection
Summary
There are more than 179.27 million confirmed coronavirus disease 2019(COVID-19) cases, with more than 5,089,384 deaths reported to WorldOmeters as of Nov. 11, 2021. There are more than 179.27 million confirmed coronavirus disease 2019. The number of countries having more than 10 million confirmed cases worldwide increased to 36. With the global outbreak of COVID-19 and the limited availability of clinical treatments, researchers around the world are looking for potential drugs to treat COVID-19 [1, 2]. Due to the severe clinical progression of COVID-19 patients with increased inflammation and immune response disorders, a considerable number of patients had severe pneumonia, and even developed acute respiratory distress syndrome (ARDS) [3]. Cytokine storm-related syndrome (IL6, IL1, TNFα, etc.) has been proposed as the trigger for ARDS. Treatments (such as corticosteroids) to control the inflammatory cytokine signaling are being used to reduce the mortality of patients with COVID-19 [4, 5]. Extracellular vesicles (EV), especially exosomes, have emerged as key mediators in various physio-pathological processes related to virus infection and are actively involved in response to virus-induced injury [6], mediating inflammatory response and inflammation-related protection, since they display dual beneficial and detrimental roles [7]
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