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Objectives: Identifying patients with COVID-19 who are at risk of poor evolution is key to early decide on their hospitalization. We evaluated the combined impact of nucleocapsid (N)-antigenemia profiled by a rapid test and antibodies against the S1 subunit of the SARS-CoV S protein (S1) on the hospitalization risk of patients with COVID-19., Methods: N-antigenemia and anti-S1 antibodies were profiled at admission to the emergency department in 146 patients with COVID-19 using the Panbio® antigen Rapid Test and the SARS-CoV-2 immunoglobulin G II Quant/SARS-CoV-2 immunoglobulin G assay from Abbott. A multivariable analysis was used to evaluate the impact of these factors on hospitalization., Results: Patients with a positive N-antigen test in plasma and anti-S1 levels <2821 arbitrary units/mL needed hospitalization more frequently (20 of 23, 87%). A total of 20 of 71 (28.2%) of those showing a negative N-antigen test and anti-S1 ≥2821 arbitrary units/mL were hospitalized for 18 of 52 (34.6%) of the patients with only one of these conditions. Patients with a positive N-antigen test and low antibody levels showed an odds ratio, 95% confidence interval, and P-value for hospitalization of 18.21, 2.74-121.18, and 0.003, respectively, and exhibited the highest mortality (30.4%)., Conclusions: Simultaneous profiling of a rapid N-antigen test in plasma and anti-S1 levels could help to early identify patients with COVID-19 needing hospitalization., Competing Interests: Declaration of competing interest JME, MDG, JFBM, FB, and RLI had filled a patent on antigenemia as a predictor of poor outcomes in COVID-19 (EP20383140). Amanda de la Fuente reports financial support was provided by Carlos III Health Institute (PFIS: FI20/00278), co-funded by the European Social Fund (ESF)/Investing in Your Future. Francisco Sanus Ferri reports that financial support was provided by the Network of Biomedical Research Centers of the Instituto de Salud Carlos III, and by “Programa de donaciones estar preparados; UNESPA” (Madrid, Spain). Tamara Postigo contract was supported by Fundació La Marató de TV3 (ajudes Econòmiques a Projectes de Recerca sobre Covid-19 - La Marató 2020, code 202108-30-31). Jesus F Bermejo-Martin has patent pending to EP20383140. Marta Dominguez-Gil has patent pending to EP20383140. Ferran Barbe has patent pending to EP20383140. Raul Lopez-Izquierdo has patent pending to EP20383140. Jose Maria Eiros has patent pending to EP20383140. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The remaining authors have no competing interest to declare., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Infection with SARS-CoV-2 has highly variable clinical manifestations, ranging from asymptomatic infection through to life-threatening disease. Host whole blood transcriptomics can offer unique insights into the biological processes underpinning infection and disease, as well as severity. We performed whole blood RNA Sequencing of individuals with varying degrees of COVID-19 severity. We used differential expression analysis and pathway enrichment analysis to explore how the blood transcriptome differs between individuals with mild, moderate, and severe COVID-19, performing pairwise comparisons between groups. Increasing COVID-19 severity was characterised by an abundance of inflammatory immune response genes and pathways, including many related to neutrophils and macrophages, in addition to an upregulation of immunoglobulin genes. In this study, for the first time, we show how immunomodulatory treatments commonly administered to COVID-19 patients greatly alter the transcriptome. Our insights into COVID-19 severity reveal the role of immune dysregulation in the progression to severe disease and highlight the need for further research exploring the interplay between SARS-CoV-2 and the inflammatory immune response., (© 2022. The Author(s).)

Coronavirus Disease-19 (COVID-19) symptoms range from mild to severe illness; the cause for this differential response to infection remains unknown. Unravelling the immune mechanisms acting at different levels of the colonization process might be key to understand these differences. We carried out a multi-tissue (nasal, buccal and blood; n = 156) gene expression analysis of immune-related genes from patients affected by different COVID-19 severities, and healthy controls through the nCounter technology. Mild and asymptomatic cases showed a powerful innate antiviral response in nasal epithelium, characterized by activation of interferon (IFN) pathway and downstream cascades, successfully controlling the infection at local level. In contrast, weak macrophage/monocyte driven innate antiviral response and lack of IFN signalling activity were present in severe cases. Consequently, oral mucosa from severe patients showed signals of viral activity, cell arresting and viral dissemination to the lower respiratory tract, which ultimately could explain the exacerbated innate immune response and impaired adaptative immune responses observed at systemic level. Results from saliva transcriptome suggest that the buccal cavity might play a key role in SARS-CoV-2 infection and dissemination in patients with worse prognosis. Co-expression network analysis adds further support to these findings, by detecting modules specifically correlated with severity involved in the abovementioned biological routes; this analysis also provides new candidate genes that might be tested as biomarkers in future studies. We also found tissue specific severity-related signatures mainly represented by genes involved in the innate immune system and cytokine/chemokine signalling. Local immune response could be key to determine the course of the systemic response and thus COVID-19 severity. Our findings provide a framework to investigate severity host gene biomarkers and pathways that might be relevant to diagnosis, prognosis, and therapy., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Emerging evidence indicates a potential role for monocytes in COVID-19 immunopathology. We investigated two soluble markers of monocyte activation, sCD14 and sCD163, in COVID-19 patients, with the aim of characterizing their potential role in monocyte-macrophage disease immunopathology. To the best of our knowledge, this is the first study of its kind. Methods: Fifty-nine SARS-Cov-2 positive hospitalized patients, classified according to ICU or non-ICU admission requirement, were prospectively recruited and analyzed by ELISA for levels of sCD14 and sCD163, along with other laboratory parameters, and compared to a healthy control group. Results: sCD14 and sCD163 levels were significantly higher among COVID-19 patients, independently of ICU admission requirement, compared to the control group. We found a significant correlation between sCD14 levels and other inflammatory markers, particularly Interleukin-6, in the non-ICU patients group. sCD163 showed a moderate positive correlation with the time lapsed from admission to sampling, independently of severity group. Treatment with corticoids showed an interference with sCD14 levels, whereas hydroxychloroquine and tocilizumab did not. Conclusions: Monocyte-macrophage activation markers are increased and correlate with other inflammatory markers in SARS-Cov-2 infection, in association to hospital admission. These data suggest a preponderant role for monocyte-macrophage activation in the development of immunopathology of COVID-19 patients. [ABSTRACT FROM AUTHOR]

• We analyze the impact of sovereign risk on banking risk in Eurozone during the COVID-19 pandemic. • Sovereign risk has impacted banking risk in Eurozone. • The transmission route is through spillovers to volatility. • There is no evidence that sovereign risk in peripheral countries has impacted in banking risk in core countries. • The impacts of both previous risks are offset. This paper studies the impact of sovereign risk on Eurozone banking risk during a novel crisis such as the COVID-19 pandemic. Spillover effects on volatility are identified using Granger causality tests, a spillover matrix, and BEKK-GARCH models. The results confirm that an increase in Eurozone sovereign risk has impacted banking risk in Eurozone and that there is no evidence that sovereign risk in the countries of the Eurozone periphery is being transmitted to banking risk in the core countries during the crisis. These conclusions are very important for risk management and the design and monitoring of Eurozone financial policies. [ABSTRACT FROM AUTHOR]