Abstract
Acute respiratory distress syndrome (ARDS) is a severe pulmonary disease, which is one of the major complications in COVID-19 patients. Dysregulation of the immune system and imbalances in cytokine release and immune cell activation are involved in SARS-CoV-2 infection. Here, the inflammatory, antigen, and auto-immune profile of patients presenting COVID-19-associated severe ARDS has been analyzed using functional proteomics approaches. Both, innate and humoral responses have been characterized through acute-phase protein network and auto-antibody signature. Severity and sepsis by SARS-CoV-2 emerged to be correlated with auto-immune profiles of patients and define their clinical progression, which could provide novel perspectives in therapeutics development and biomarkers of COVID-19 patients. Humoral response in COVID-19 patients’ profile separates with significant differences patients with or without ARDS. Furthermore, we found that this profile can be correlated with COVID-19 severity and results more common in elderly patients.
Highlights
Coronaviruses (CoV) are a family of single-stranded positive RNA viruses with high diversity
In the search to cross-check all the immune profiles of patients with Acute respiratory distress syndrome (ARDS) in COVID-19, this study has begun by analyzing the antigenic profile related to SARS-CoV-2, and to other CoVs to collect a complete antigenic profile for this type of viruses
Antigenic multiplex assay for other coronaviruses (Figure 1) indicates that 87% has S1 protein antibodies for CoV-229E, 97% for CoV-HKU1, 90% for CoV-OC43, 97% for CoV-NL63, and 33% for SARS-CoV
Summary
Coronaviruses (CoV) are a family of single-stranded positive RNA viruses with high diversity. This family is classified into three groups: Alphacoronavirus, Betacoronavirus and Gammacoronavirus. Seven types of CoVs are known to be capable of infecting humans, two Alphacoronavirus (CoV-229E and CoV-NL63) and five Betacoronavirus (CoV-HKU1, CoV-OC43, SARS-CoV, MERS-CoV, and SARS-CoV-2) [1,2,3]. It is interesting to note that all CoVs have common characteristics. Their structural proteins include the spike glycoprotein (S), responsible for virus–host cell interaction; envelope (E) and membrane (M), accountable for the formation of the viral envelope and nucleocapsid (N), in charge
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