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1.
Biomed Pharmacother ; 145: 112419, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1574950

ABSTRACT

Interleukin-6 (IL-6) is a multi-tasking cytokine that represents high activity in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and cancer. High concentration of this pleiotropic cytokine accounts for hyperinflammation and cytokine storm, and is related to multi-organ failure in patients with SARS-CoV-2 induced disease. IL-6 promotes lymphopenia and increases C-reactive protein (CRP) in such cases. However, blockade of IL-6 is not a full-proof of complete response. Hypoxia, hypoxemia, aberrant angiogenesis and chronic inflammation are inter-related events occurring as a response to the SARS-CoV-2 stimulatory effect on high IL-6 activity. Taking both pro- and anti-inflammatory activities will make complex targeting IL-6 in patient with SARS-CoV-2 induced disease. The aim of this review was to discuss about interactions occurring within the body of patients with SARS-CoV-2 induced disease who are representing high IL-6 levels, and to determine whether IL-6 inhibition therapy is effective for such patients or not. We also address the interactions and targeted therapies in cancer patients who also have SARS-CoV-2 induced disease.


Subject(s)
COVID-19 , Immune Checkpoint Inhibitors/pharmacology , Interleukin-6 , Multiple Organ Failure , Neoplasms , Antibodies, Monoclonal, Humanized/pharmacology , COVID-19/complications , COVID-19/drug therapy , COVID-19/immunology , Humans , Interleukin-6/antagonists & inhibitors , Interleukin-6/immunology , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology , Neoplasms/complications , Neoplasms/drug therapy , Neoplasms/immunology , SARS-CoV-2
2.
Viral Immunol ; 34(10): 679-688, 2021 12.
Article in English | MEDLINE | ID: covidwho-1560640

ABSTRACT

The newfound coronavirus disease 2019 (COVID-19), initiated by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is an international public health concern, threatening the lives of millions of people worldwide. The virus seems to have a propensity to infect older males, especially those with underlying diseases. The cytokine storm following hyperactivated immune responses due to SARS-CoV-2 infection is probably the crucial source of severe pneumonia that leads to acute lung injury, systemic inflammatory response syndrome, or acute respiratory distress syndrome, and finally multiple organ dysfunction syndromes, as well as death in many cases. Several studies revealed that interleukin (IL)-1ß levels were elevated during COVID-19 infection. In addition, the IL-1 cytokine family has a pivotal role in the induction of cytokine storm due to uncontrolled immune responses in COVID-19 infection. This article reviews the role of IL-1 in inflammation and utilization of IL-1 inhibitor agents in controlling the inflammatory outcomes initiated by SARS-CoV-2 infection.


Subject(s)
COVID-19/drug therapy , COVID-19/immunology , Cytokine Release Syndrome/drug therapy , Interleukin-1/immunology , Acute Lung Injury/drug therapy , Acute Lung Injury/immunology , Acute Lung Injury/pathology , COVID-19/mortality , COVID-19/pathology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/pathology , Humans , Interleukin-1/antagonists & inhibitors , Multiple Organ Failure/drug therapy , Multiple Organ Failure/immunology , Multiple Organ Failure/pathology , Respiratory Distress Syndrome/drug therapy , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/pathology , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity
3.
Cells ; 10(11)2021 10 25.
Article in English | MEDLINE | ID: covidwho-1480601

ABSTRACT

As the number of confirmed cases and deaths occurring from Coronavirus disease 2019 (COVID-19) surges worldwide, health experts are striving hard to fully comprehend the extent of damage caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although COVID-19 primarily manifests itself in the form of severe respiratory distress, it is also known to cause systemic damage to almost all major organs and organ systems within the body. In this review, we discuss the molecular mechanisms leading to multi-organ failure seen in COVID-19 patients. We also examine the potential of stem cell therapy in treating COVID-19 multi-organ failure cases.


Subject(s)
COVID-19/complications , COVID-19/therapy , Multiple Organ Failure/etiology , Multiple Organ Failure/therapy , Stem Cell Transplantation , COVID-19/immunology , Clinical Trials as Topic , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/therapy , Humans , Immunomodulation , Multiple Organ Failure/immunology , Regenerative Medicine , SARS-CoV-2/pathogenicity , Stem Cells/cytology , Stem Cells/immunology
4.
Immunopharmacol Immunotoxicol ; 43(6): 633-643, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1467231

ABSTRACT

The coronavirus disease-19 (COVID-19), at first, was reported in Wuhan, China, and then rapidly became pandemic throughout the world. Cytokine storm syndrome (CSS) in COVID-19 patients is associated with high levels of cytokines and chemokines that cause multiple organ failure, systemic inflammation, and hemodynamic instabilities. Acute respiratory distress syndrome (ARDS), a common complication of COVID-19, is a consequence of cytokine storm. In this regard, several drugs have been being investigated to suppress this inflammatory condition. Purinergic signaling receptors comprising of P1 adenosine and P2 purinoceptors play a critical role in inflammation. Therefore, activation or inhibition of some subtypes of these kinds of receptors is most likely to be beneficial to attenuate cytokine storm. This article summarizes suggested therapeutic drugs with potential anti-inflammatory effects through purinergic receptors.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , COVID-19/drug therapy , Cytokine Release Syndrome/prevention & control , Cytokines/blood , Purinergic Antagonists/therapeutic use , Receptors, Purinergic/drug effects , SARS-CoV-2/drug effects , Animals , Anti-Inflammatory Agents/adverse effects , Biomarkers/blood , COVID-19/blood , COVID-19/immunology , COVID-19/virology , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/virology , Host-Pathogen Interactions , Humans , Ligands , Molecular Targeted Therapy , Multiple Organ Failure/immunology , Multiple Organ Failure/prevention & control , Multiple Organ Failure/virology , Purinergic Antagonists/adverse effects , Receptors, Purinergic/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Signal Transduction
5.
Mayo Clin Proc ; 96(12): 3099-3108, 2021 12.
Article in English | MEDLINE | ID: covidwho-1364351

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible virus with significant global impact, morbidity, and mortality. The SARS-CoV-2 virus may result in widespread organ manifestations including acute respiratory distress syndrome, acute renal failure, thromboembolism, and myocarditis. Virus-induced endothelial injury may cause endothelial activation, increased permeability, inflammation, and immune response and cytokine storm. Endothelial dysfunction is a systemic disorder that is a precursor of atherosclerotic vascular disease that is associated with cardiovascular risk factors and is highly prevalent in patients with atherosclerotic cardiovascular and peripheral disease. Several studies have associated various viral infections including SARS-CoV-2 infection with inflammation, endothelial dysfunction, and subsequent innate immune response and cytokine storm. Noninvasive monitoring of endothelial function and identification of high-risk patients who may require specific therapies may have the potential to improve morbidity and mortality associated with subsequent inflammation, cytokine storm, and multiorgan involvement.


Subject(s)
COVID-19 , Endothelium , COVID-19/immunology , COVID-19/physiopathology , Cytokine Release Syndrome/virology , Disease Management , Endothelium/physiopathology , Endothelium/virology , Humans , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology , SARS-CoV-2/physiology , Systemic Inflammatory Response Syndrome/prevention & control , Systemic Inflammatory Response Syndrome/virology
6.
Int J Mol Sci ; 22(15)2021 Jul 24.
Article in English | MEDLINE | ID: covidwho-1325681

ABSTRACT

The outbreak of the coronavirus disease 2019 (COVID-19) began at the end of 2019. COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with COVID-19 may exhibit poor clinical outcomes. Some patients with severe COVID-19 experience cytokine release syndrome (CRS) or a cytokine storm-elevated levels of hyperactivated immune cells-and circulating pro-inflammatory cytokines, including interleukin (IL)-1ß and IL-18. This severe inflammatory response can lead to organ damage/failure and even death. The inflammasome is an intracellular immune complex that is responsible for the secretion of IL-1ß and IL-18 in various human diseases. Recently, there has been a growing number of studies revealing a link between the inflammasome and COVID-19. Therefore, this article summarizes the current literature regarding the inflammasome complex and COVID-19.


Subject(s)
COVID-19/immunology , COVID-19/virology , Inflammasomes/immunology , Inflammasomes/metabolism , SARS-CoV-2/immunology , SARS-CoV-2/metabolism , Adaptive Immunity/immunology , Animals , COVID-19/complications , COVID-19/drug therapy , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/immunology , Humans , Multiple Organ Failure/drug therapy , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology
7.
Pediatr Infect Dis J ; 40(7): e259-e262, 2021 07 01.
Article in English | MEDLINE | ID: covidwho-1258812

ABSTRACT

Multisystem inflammatory syndrome in children (MIS-C) associated with SARS-CoV-2 infection is an infrequent and poorly understood illness. It can present as severe multiorgan failure in children, potentially lethal. Immunomodulation is the empiric treatment because a dysregulated immune response is the primary pathophysiologic mechanism. We present an infant with severe MIS-C, refractory to usual treatment, successfully treated with plasmapheresis.


Subject(s)
COVID-19/therapy , Immunomodulation , Multiple Organ Failure/immunology , Multiple Organ Failure/therapy , Plasma Exchange , Systemic Inflammatory Response Syndrome/therapy , Child, Preschool , Female , Humans , Treatment Outcome
8.
Pharmacol Res ; 168: 105581, 2021 06.
Article in English | MEDLINE | ID: covidwho-1157664

ABSTRACT

In-depth characterization of heart-brain communication in critically ill patients with severe acute respiratory failure is attracting significant interest in the COronaVIrus Disease 19 (COVID-19) pandemic era during intensive care unit (ICU) stay and after ICU or hospital discharge. Emerging research has provided new insights into pathogenic role of the deregulation of the heart-brain axis (HBA), a bidirectional flow of information, in leading to severe multiorgan disease syndrome (MODS) in patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Noteworthy, HBA dysfunction may worsen the outcome of the COVID-19 patients. In this review, we discuss the critical role HBA plays in both promoting and limiting MODS in COVID-19. We also highlight the role of HBA as new target for novel therapeutic strategies in COVID-19 in order to open new translational frontiers of care. This is a translational perspective from the Italian Society of Cardiovascular Researches.


Subject(s)
Brain Diseases/therapy , Brain/drug effects , COVID-19/therapy , Heart Diseases/therapy , Heart/drug effects , Adrenal Cortex Hormones/administration & dosage , Anti-Inflammatory Agents/administration & dosage , Antiviral Agents/administration & dosage , Brain/immunology , Brain/metabolism , Brain Diseases/immunology , Brain Diseases/metabolism , COVID-19/immunology , COVID-19/metabolism , Critical Care/methods , Critical Illness/therapy , Dietary Supplements , Functional Food , Heart Diseases/immunology , Heart Diseases/metabolism , Humans , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Microvessels/drug effects , Microvessels/immunology , Microvessels/metabolism , Multiple Organ Failure/immunology , Multiple Organ Failure/metabolism , Multiple Organ Failure/therapy , SARS-CoV-2/drug effects , SARS-CoV-2/immunology , SARS-CoV-2/metabolism
9.
Am J Respir Crit Care Med ; 203(2): 192-201, 2021 01 15.
Article in English | MEDLINE | ID: covidwho-1059843

ABSTRACT

Rationale: In life-threatening coronavirus disease (COVID-19), corticosteroids reduce mortality, suggesting that immune responses have a causal role in death. Whether this deleterious inflammation is primarily a direct reaction to the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or an independent immunopathologic process is unknown.Objectives: To determine SARS-CoV-2 organotropism and organ-specific inflammatory responses and the relationships among viral presence, inflammation, and organ injury.Methods: Tissue was acquired from 11 detailed postmortem examinations. SARS-CoV-2 organotropism was mapped by using multiplex PCR and sequencing, with cellular resolution achieved by in situ viral S (spike) protein detection. Histologic evidence of inflammation was quantified from 37 anatomic sites, and the pulmonary immune response was characterized by using multiplex immunofluorescence.Measurements and Main Results: Multiple aberrant immune responses in fatal COVID-19 were found, principally involving the lung and reticuloendothelial system, and these were not clearly topologically associated with the virus. Inflammation and organ dysfunction did not map to the tissue and cellular distribution of SARS-CoV-2 RNA and protein between or within tissues. An arteritis was identified in the lung, which was further characterized as a monocyte/myeloid-rich vasculitis, and occurred together with an influx of macrophage/monocyte-lineage cells into the pulmonary parenchyma. In addition, stereotyped abnormal reticuloendothelial responses, including excessive reactive plasmacytosis and iron-laden macrophages, were present and dissociated from viral presence in lymphoid tissues.Conclusions: Tissue-specific immunopathology occurs in COVID-19, implicating a significant component of the immune-mediated, virus-independent immunopathologic process as a primary mechanism in severe disease. Our data highlight novel immunopathologic mechanisms and validate ongoing and future efforts to therapeutically target aberrant macrophage and plasma-cell responses as well as promote pathogen tolerance in COVID-19.


Subject(s)
COVID-19/immunology , Inflammation/virology , Lung/immunology , Multiple Organ Failure/virology , SARS-CoV-2/immunology , Aged , Aged, 80 and over , Autopsy , Biopsy , COVID-19/pathology , COVID-19/virology , COVID-19 Nucleic Acid Testing , Female , Fluorescent Antibody Technique , Humans , Inflammation/immunology , Inflammation/pathology , Lung/pathology , Lung/virology , Male , Multiple Organ Failure/immunology , Multiple Organ Failure/pathology , SARS-CoV-2/pathogenicity , Severity of Illness Index
10.
Am J Respir Crit Care Med ; 203(2): 192-201, 2021 01 15.
Article in English | MEDLINE | ID: covidwho-939947

ABSTRACT

Rationale: In life-threatening coronavirus disease (COVID-19), corticosteroids reduce mortality, suggesting that immune responses have a causal role in death. Whether this deleterious inflammation is primarily a direct reaction to the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or an independent immunopathologic process is unknown.Objectives: To determine SARS-CoV-2 organotropism and organ-specific inflammatory responses and the relationships among viral presence, inflammation, and organ injury.Methods: Tissue was acquired from 11 detailed postmortem examinations. SARS-CoV-2 organotropism was mapped by using multiplex PCR and sequencing, with cellular resolution achieved by in situ viral S (spike) protein detection. Histologic evidence of inflammation was quantified from 37 anatomic sites, and the pulmonary immune response was characterized by using multiplex immunofluorescence.Measurements and Main Results: Multiple aberrant immune responses in fatal COVID-19 were found, principally involving the lung and reticuloendothelial system, and these were not clearly topologically associated with the virus. Inflammation and organ dysfunction did not map to the tissue and cellular distribution of SARS-CoV-2 RNA and protein between or within tissues. An arteritis was identified in the lung, which was further characterized as a monocyte/myeloid-rich vasculitis, and occurred together with an influx of macrophage/monocyte-lineage cells into the pulmonary parenchyma. In addition, stereotyped abnormal reticuloendothelial responses, including excessive reactive plasmacytosis and iron-laden macrophages, were present and dissociated from viral presence in lymphoid tissues.Conclusions: Tissue-specific immunopathology occurs in COVID-19, implicating a significant component of the immune-mediated, virus-independent immunopathologic process as a primary mechanism in severe disease. Our data highlight novel immunopathologic mechanisms and validate ongoing and future efforts to therapeutically target aberrant macrophage and plasma-cell responses as well as promote pathogen tolerance in COVID-19.


Subject(s)
COVID-19/immunology , Inflammation/virology , Lung/immunology , Multiple Organ Failure/virology , SARS-CoV-2/immunology , Aged , Aged, 80 and over , Autopsy , Biopsy , COVID-19/pathology , COVID-19/virology , COVID-19 Nucleic Acid Testing , Female , Fluorescent Antibody Technique , Humans , Inflammation/immunology , Inflammation/pathology , Lung/pathology , Lung/virology , Male , Multiple Organ Failure/immunology , Multiple Organ Failure/pathology , SARS-CoV-2/pathogenicity , Severity of Illness Index
11.
Mediators Inflamm ; 2020: 8198963, 2020.
Article in English | MEDLINE | ID: covidwho-829084

ABSTRACT

The novel coronavirus is not only causing respiratory problems, but it may also damage the heart, kidneys, liver, and other organs; in Wuhan, 14 to 30% of COVID-19 patients have lost their kidney function and now require either dialysis or kidney transplants. The novel coronavirus gains entry into humans by targeting the ACE2 receptor that found on lung cells, which destroy human lungs through cytokine storms, and this leads to hyperinflammation, forcing the immune cells to destroy healthy cells. This is why some COVID-19 patients need intensive care. The inflammatory chemicals released during COVID-19 infection cause the liver to produce proteins that defend the body from infections. However, these proteins can cause blood clotting, which can clog blood vessels in the heart and other organs; as a result, the organs are deprived of oxygen and nutrients which could ultimately lead to multiorgan failure and consequent progression to acute lung injury, acute respiratory distress syndrome, and often death. However, there are novel protein modification tools called the QTY code, which are similar in their structure to antibodies, which could provide a solution to excess cytokines. These synthetic proteins can be injected into the body to bind the excess cytokines created by the cytokine storm; this will eventually remove the excessive cytokines and inhibit the severe symptoms caused by the COVID-19 infection. In this review, we will focus on cytokine storm in COVID-19 patients, their impact on the body organs, and the potential treatment by QTY code-designed detergent-free chemokine receptors.


Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/immunology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/therapy , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Receptors, Chemokine/therapeutic use , Betacoronavirus , COVID-19 , Coronavirus Infections/drug therapy , Coronavirus Infections/therapy , Cytokine Release Syndrome/immunology , Cytokines/antagonists & inhibitors , Drug Design , Humans , Inflammation Mediators/blood , Inflammation Mediators/immunology , Models, Molecular , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology , Multiple Organ Failure/therapy , Pandemics , Pneumonia, Viral/therapy , Protein Engineering , Protein Modification, Translational , Receptors, Chemokine/genetics , Receptors, Chemokine/metabolism , SARS-CoV-2
12.
J Immunol ; 205(10): 2566-2575, 2020 11 15.
Article in English | MEDLINE | ID: covidwho-789578

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which rapidly became a pandemic of global proportions. Sepsis is commonly present with high lethality in the severe forms of the disease. The virus-induced cytokine storm puts the immune system in overdrive at the expense of the pathogen-specific immune response and is likely to underlie the most advanced COVID-19 clinical features, including sepsis-related multiple organ dysfunction as well as the pathophysiological changes found in the lungs. We review the major therapeutic strategies that have been considered for sepsis and might be amenable to repurposing for COVID-19. We also discuss two different immunization strategies that have the potential to confer antiviral heterologous protection: innate-induced trained immunity and adaptive-induced immune response resetting.


Subject(s)
Adaptive Immunity , Betacoronavirus/immunology , Coronavirus Infections , Cytokines/immunology , Immunity, Innate , Multiple Organ Failure , Pandemics , Pneumonia, Viral , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/pathology , Coronavirus Infections/therapy , Humans , Multiple Organ Failure/immunology , Multiple Organ Failure/pathology , Multiple Organ Failure/therapy , Pneumonia, Viral/immunology , Pneumonia, Viral/pathology , Pneumonia, Viral/therapy , SARS-CoV-2
13.
Respir Physiol Neurobiol ; 283: 103548, 2021 01.
Article in English | MEDLINE | ID: covidwho-779595

ABSTRACT

BACKGROUND: Globally, the current medical emergency for novel coronavirus 2019 (COVID-19) leads to respiratory distress syndrome and death. PURPOSE: This review highlighted the effect of COVID-19 on systemic multiple organ failure syndromes. This review is intended to fill a gap in information about human physiological response to COVID-19 infections. This review may shed some light on other potential mechanisms and approaches in COVID -19 infections towards systemic multiorgan failure syndromes. FINDING: SARS-CoV-2 intervened mainly in the lung with progression to pneumonia and acute respiratory distress syndrome (ARDS) via the angiotensin-converting enzyme 2(ACE2) receptor. Depending on the viral load, infection spread through the ACE2 receptor further to various organs such as heart, liver, kidney, brain, endothelium, GIT, immune cell, and RBC (thromboembolism). This may be aggravated by cytokine storm with the extensive release of proinflammatory cytokines from the deregulating immune system. CONCLUSION: The widespread and vicious combinations of cytokines with organ crosstalk contribute to systemic hyper inflammation and ultimately lead to multiple organ dysfunction (Fig. 1). This comprehensive study comprises various manifestations of different organs in COVID-19 and may assist the clinicians and scientists pertaining to a broad approach to fight COVID 19.


Subject(s)
Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Multiple Organ Failure/immunology , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/immunology , Respiratory Distress Syndrome/immunology , Spike Glycoprotein, Coronavirus/metabolism , Acute Kidney Injury/immunology , Acute Kidney Injury/physiopathology , Angiotensin-Converting Enzyme 2 , Arrhythmias, Cardiac/immunology , Arrhythmias, Cardiac/physiopathology , Betacoronavirus/metabolism , COVID-19 , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/physiopathology , Cytokines/immunology , Endothelium, Vascular/metabolism , Erythrocytes/metabolism , Gastrointestinal Diseases/immunology , Gastrointestinal Diseases/physiopathology , Gastrointestinal Tract/metabolism , Heart Failure/immunology , Heart Failure/physiopathology , Humans , Inflammation/immunology , Kidney/metabolism , Liver/metabolism , Liver Diseases/immunology , Liver Diseases/physiopathology , Lung/metabolism , Multiple Organ Failure/physiopathology , Myocardium/metabolism , Pandemics , Pneumonia, Viral/physiopathology , Respiratory Distress Syndrome/physiopathology , SARS-CoV-2 , Thromboembolism/immunology , Thromboembolism/physiopathology , Viral Load
15.
J Clin Immunol ; 40(8): 1082-1092, 2020 11.
Article in English | MEDLINE | ID: covidwho-724903

ABSTRACT

We report a longitudinal analysis of the immune response associated with a fatal case of COVID-19 in Europe. This patient exhibited a rapid evolution towards multiorgan failure. SARS-CoV-2 was detected in multiple nasopharyngeal, blood, and pleural samples, despite antiviral and immunomodulator treatment. Clinical evolution in the blood was marked by an increase (2-3-fold) in differentiated effector T cells expressing exhaustion (PD-1) and senescence (CD57) markers, an expansion of antibody-secreting cells, a 15-fold increase in γδ T cell and proliferating NK-cell populations, and the total disappearance of monocytes, suggesting lung trafficking. In the serum, waves of a pro-inflammatory cytokine storm, Th1 and Th2 activation, and markers of T cell exhaustion, apoptosis, cell cytotoxicity, and endothelial activation were observed until the fatal outcome. This case underscores the need for well-designed studies to investigate complementary approaches to control viral replication, the source of the hyperinflammatory status, and immunomodulation to target the pathophysiological response. The investigation was conducted as part of an overall French clinical cohort assessing patients with COVID-19 and registered in clinicaltrials.gov under the following number: NCT04262921.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/complications , Cytokine Release Syndrome/immunology , Multiple Organ Failure/immunology , Pneumonia, Viral/complications , Respiratory Distress Syndrome/immunology , Aged, 80 and over , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/therapy , Cytokine Release Syndrome/virology , Fatal Outcome , France , Humans , Longitudinal Studies , Lymphocyte Activation , Male , Multiple Organ Failure/blood , Multiple Organ Failure/therapy , Multiple Organ Failure/virology , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Prospective Studies , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/therapy , Respiratory Distress Syndrome/virology , SARS-CoV-2 , Severity of Illness Index , T-Lymphocytes, Cytotoxic/immunology , Th1 Cells/immunology , Th2 Cells/immunology
16.
Curr Probl Cardiol ; 45(8): 100618, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-694853

ABSTRACT

Since the outbreak and rapid spread of COVID-19 starting late December 2019, it has been apparent that disease prognosis has largely been influenced by multiorgan involvement. Comorbidities such as cardiovascular diseases have been the most common risk factors for severity and mortality. The hyperinflammatory response of the body, coupled with the plausible direct effects of severe acute respiratory syndrome on body-wide organs via angiotensin-converting enzyme 2, has been associated with complications of the disease. Acute respiratory distress syndrome, heart failure, renal failure, liver damage, shock, and multiorgan failure have precipitated death. Acknowledging the comorbidities and potential organ injuries throughout the course of COVID-19 is therefore crucial in the clinical management of patients. This paper aims to add onto the ever-emerging landscape of medical knowledge on COVID-19, encapsulating its multiorgan impact.


Subject(s)
Cardiovascular Diseases/epidemiology , Coronavirus Infections , Multiple Organ Failure , Pandemics , Pneumonia, Viral , Angiotensin-Converting Enzyme 2 , Betacoronavirus/physiology , COVID-19 , Comorbidity , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Humans , Multiple Organ Failure/etiology , Multiple Organ Failure/immunology , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , Risk Factors , SARS-CoV-2
17.
Clin Sci (Lond) ; 134(12): 1295-1300, 2020 06 26.
Article in English | MEDLINE | ID: covidwho-599624

ABSTRACT

We demonstrate that the general clinical conditions, risk factors and numerous pathological and biological features of COVID-19 are analogous with various disorders caused by the uncontrolled formation of neutrophil extracellular traps and their by-products. Given the rapid evolution of this disease's symptoms and its lethality, we hypothesize that SARS-CoV2 evades innate immune response causing COVID-19 progresses under just such an amplifier loop, leading to a massive, uncontrolled inflammation process. This work allows us to propose new strategies for treating the pandemic.


Subject(s)
Betacoronavirus/physiology , Coronavirus Infections/immunology , Extracellular Traps/physiology , Host-Pathogen Interactions/immunology , Pneumonia, Viral/immunology , COVID-19 , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Deoxyribonuclease I/therapeutic use , Humans , Immunity, Innate , Multiple Organ Failure/immunology , Multiple Organ Failure/virology , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , SARS-CoV-2
19.
Life Sci ; 256: 117900, 2020 Sep 01.
Article in English | MEDLINE | ID: covidwho-459105

ABSTRACT

AIM: Coronavirus disease 2019 (COVID-19) is a novel highly contagious infection caused by SARS-CoV-2, which has been became a global public health challenge. The pathogenesis of this virus is not yet clearly understood, but there is evidence of a hyper-inflammatory immune response in critically ill patients, which leads to acute respiratory distress syndrome (ARDS) and multi-organ failure. MATERIAL AND METHODS: A literature review was performed to identify relevant articles on COVID-19 published up to April 30, 2020. The search resulted in 361 total articles. After reviewing the titles and abstracts for inclusion, some irrelevant papers were excluded. Additional relevant articles were identified from a review of citations referenced. KEY FINDINGS: SARS-CoV-2, directly and indirectly, affects the immune system and avoids being eliminated in early stages. On the other hand, the secretion of inflammatory cytokines creates critical conditions that lead to multi-organ failure. SIGNIFICANCE: The immune system which is affected by the virus tries to respond via a cytokine storm and hyperinflammation, which itself leads to further multi-organ damage and even death.


Subject(s)
Betacoronavirus/immunology , Coronavirus Infections/physiopathology , Immune System/virology , Pneumonia, Viral/physiopathology , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/immunology , Coronavirus Infections/virology , Critical Illness , Cytokines/immunology , Humans , Multiple Organ Failure/immunology , Multiple Organ Failure/virology , Pandemics , Pneumonia, Viral/immunology , Pneumonia, Viral/virology , Respiratory Distress Syndrome/immunology , Respiratory Distress Syndrome/virology , SARS-CoV-2
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