COVID-19: Integrating the Complexity of Systemic and Pulmonary Immunopathology to Identify Biomarkers for Different Outcomes.

Thais Fernanda De Campos Fraga-Silva,Ana Paula Morais Fernandes,Sandra Regina Maruyama,Cristina Ribeiro De Barros Cardoso,Lucia Helena Faccioli,Elisa Maria De Sousa Russo,Marcelo Dias-Baruffi,Carlos Arterio Sorgi,Vânia Luiza Deperon Bonato

doi:10.3389/fimmu.2020.599736

Thais Fernanda De Campos Fraga-Silva, Ana Paula Morais Fernandes + Show 7 more

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https://doi.org/10.3389/fimmu.2020.599736

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In the last few months, the coronavirus disease 2019 (COVID-19) pandemic has affected millions of people worldwide and has provoked an exceptional effort from the scientific community to understand the disease. Clinical evidence suggests that severe COVID-19 is associated with both dysregulation of damage tolerance caused by pulmonary immunopathology and high viral load. In this review article, we describe and discuss clinical studies that show advances in the understanding of mild and severe illness and we highlight major points that are critical for improving the comprehension of different clinical outcomes. The understanding of pulmonary immunopathology will contribute to the identification of biomarkers in an attempt to classify mild, moderate, severe and critical COVID-19 illness. The interface of pulmonary immunopathology and the identification of biomarkers are critical for the development of new therapeutic strategies aimed to reduce the systemic and pulmonary hyperinflammation in severe COVID-19.

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Between the end of December 2019 and the beginning 2020 a progressive number of deaths due to aggressive pneumonia in the province of Wuhan, China, led to the identification of a new coronavirus, called Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), as the cause of Coronavirus Disease 2019 (COVID-19) [1,2,3]
During epidemics resulting from coronavirus infections in 2002/ 2003 (Severe Acute Respiratory Syndrome Coronavirus - SARSCoV) and 2012/2013 (Middle East Respiratory Syndrome MERS), respectively, researchers suggested, based on lung histopathological analysis from individuals who died of pulmonary disease, that the progressive and late form of severe acute respiratory syndrome (SARS)-CoV disease was more associated with tissue damage caused by immunopathology than with viral load [63]
In contrast to the results reported by Dorward and coworkers [7], a high viral RNA load was associated with high expression of IFN pathway, endothelial and wound healing genes, which corroborate the findings of lung damage characterized by exudative diffuse alveolar damage, fibrosis, infiltration of macrophages, monocytes, T cells and NK cells in areas positive or negative for SARS-CoV-2, and high expression of CTLA-4, PD-L1, and IDO

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Introduction

Between the end of December 2019 and the beginning 2020 a progressive number of deaths due to aggressive pneumonia in the province of Wuhan, China, led to the identification of a new coronavirus, called Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), as the cause of Coronavirus Disease 2019 (COVID-19) [1,2,3]. The analysis of 700 lung transcriptome samples of patients with comorbidities associated with COVID-19, such as hypertension, chronic obstructive pulmonary disease (COPD) and diabetes, showed that the expression of ACE-2 receptor was higher in those patients compared to controls [17].

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