SARS-CoV-2 infection: Understanding the immune system abnormalities to get an adequate diagnosis.

Karen Medina-Quero,Voltaire Mendez-Rodriguez,Omar Barreto-Rodriguez,Leslie Chavez-Galan,Anahí Sanchez-Moncivais,Ivette Buendia-Roldan

doi:10.17305/bjbms.2020.5400

Karen Medina-Quero, Voltaire Mendez-Rodriguez + Show 4 more

Open Access

https://doi.org/10.17305/bjbms.2020.5400

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Abstract

COVID-19 is a current pandemic that emerged from China at the end of December 2019. Its aetiological agent is the novel coronavirus SARS-CoV-2. To identify biomarkers, diagnostic tools, treatments, or vaccines to decrease COVID-19 incidence and mortality, the scientific community is making extraordinary efforts to understand all aspects of this pathogen, from viral structure to the pathophysiology and immunological processes activated in the host. Diverse abnormalities have been found during SARS-CoV-2 infection both in lymphoid and myeloid cells. Such abnormalities can disturb the immune system function and cause a massive inflammatory response that impairs tissue function. This review discusses the close relationship between immune system abnormalities and the broad spectrum of clinical manifestations, including fibrosis, in the context of COVID-19 disease. Moreover, we have described the current strategies for COVID-19 diagnosis, and we provide a summary of the most useful clinical parameters to identify severe COVID-19 patients.

Highlights

In late December 2019, an unexpected pandemic emerged from Wuhan, China; patients began to show pneumonia of unknown cause
The virus was designated as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which is the etiologic agent of the coronavirus disease 2019, hereafter called COVID-19
The reduction of non-classical and transitional monocyte frequency is associated with increased expression of IL-6. This reduction may be associated with the selective recruitment of these populations to the lung [40]. These results suggest that inflammation is transitional and non-classical monocytes preferentially migrate from blood to lungs in patients with severe COVID-19

Summary

INTRODUCTION

In late December 2019, an unexpected pandemic emerged from Wuhan, China; patients began to show pneumonia of unknown cause. Macrophages are one of the most important cell types that can induce the pro-inflammatory cytokine storm since it has been demonstrated that all COVID-19 patients with severe respiratory failure display ARDS or macrophage-activation syndrome (MAS) These complications induce an immune deregulation characterised by low HLA-DR expression on monocytes and macrophages, which is triggered by monocyte hyperactivation that promotes an excessive release of IL-6 [31,45]. Some examples of how the basic information is related to the clinical parameters are: 1) the cytokine storm (for instance, high IL-6 levels in severe condition) is a result of an imbalance on T cells subsets, 2) the pro-inflammatory macrophage subpopulation is increased in severe but not in mild disease, 3) NETs generation promotes a hypercoagulation state and microvascular damage and, 4) ACE2 is expressed on the cell surface of several cells, including enterocytes which could explain clinical manifestations such as gastrointestinal complications.

Meaning and Outcome

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Findings