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1.
Cephalalgia ; 40(13): 1410-1421, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-33146036

RESUMO

OBJECTIVE: To define headache characteristics and evolution in relation to COVID-19 and its inflammatory response. METHODS: This is a prospective study, comparing clinical data and inflammatory biomarkers of COVID-19 patients with and without headache, recruited at the Emergency Room. We compared baseline with 6-week follow-up to evaluate disease evolution. RESULTS: Of 130 patients, 74.6% (97/130) had headache. In all, 24.7% (24/97) of patients had severe pain with migraine-like features. Patients with headache had more anosmia/ageusia (54.6% vs. 18.2%; p < 0.0001). Clinical duration of COVID-19 was shorter in the headache group (23.9 ± 11.6 vs. 31.2 ± 12.0 days; p = 0.028). In the headache group, IL-6 levels were lower at the ER (22.9 (57.5) vs. 57.0 (78.6) pg/mL; p = 0.036) and more stable during hospitalisation. After 6 weeks, of 74 followed-up patients with headache, 37.8% (28/74) had ongoing headache. Of these, 50% (14/28) had no previous headache history. Headache was the prodromal symptom of COVID-19 in 21.4% (6/28) of patients with persistent headache (p = 0.010). CONCLUSIONS: Headache associated with COVID-19 is a frequent symptom, predictive of a shorter COVID-19 clinical course. Disabling headache can persist after COVID-19 resolution. Pathophysiologically, its migraine-like features may reflect an activation of the trigeminovascular system by inflammation or direct involvement of SARS-CoV-2, a hypothesis supported by concomitant anosmia.


Assuntos
Infecções por Coronavirus/complicações , Cefaleia/virologia , Pneumonia Viral/complicações , Adulto , Idoso , Betacoronavirus , Biomarcadores/sangue , Infecções por Coronavirus/imunologia , Feminino , Cefaleia/epidemiologia , Humanos , Inflamação/sangue , Inflamação/virologia , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/imunologia , Sintomas Prodrômicos , Estudos Prospectivos
2.
Anatol J Cardiol ; 24(4): 224-234, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33001051

RESUMO

Coronavirus disease 2019 (COVID-19) caused by 'Severe Acute Respiratory Syndrome Coronavirus-2' (SARS-CoV-2) infection emerged in Wuhan, a city of China, and spread to the entire planet in early 2020. The virus enters the respiratory tract cells and other tissues via ACE2 receptors. Approximately 20% of infected subjects develop severe or critical disease. A cytokine storm leads to over inflammation and thrombotic events. The most common clinical presentation in COVID-19 is pneumonia, typically characterized by bilateral, peripheral, and patchy infiltrations in the lungs. However multi-systemic involvement including peripheral thromboembolic skin lesions, central nervous, gastrointestinal, circulatory, and urinary systems are reported. The disease has a higher mortality compared to other viral agents causing pneumonia and unfortunately, no approved specific therapy, nor vaccine has yet been discovered. Several clinical trials are ongoing with hydroxychloroquine, remdesivir, favipiravir, and low molecular weight heparins. This comprehensive review aimed to summarize coagulation abnormalities reported in COVID-19, discuss the thrombosis, and inflammation-driven background of the disease, emphasize the impact of thrombotic and inflammatory processes on the progression and prognosis of COVID-19, and to provide evidence-based therapeutic guidance, especially from antithrombotic and anti-inflammatory perspectives.


Assuntos
Betacoronavirus/patogenicidade , Infecções por Coronavirus/complicações , Inflamação/virologia , Pneumonia Viral/complicações , Trombose/virologia , Transtornos da Coagulação Sanguínea/terapia , Transtornos da Coagulação Sanguínea/virologia , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/terapia , Infecções por Coronavirus/virologia , Citocinas/metabolismo , Transtornos Hemostáticos/virologia , Humanos , Imunomodulação/fisiologia , Inflamação/terapia , Pandemias , Pneumonia Viral/mortalidade , Pneumonia Viral/terapia , Pneumonia Viral/virologia , Prognóstico , Trombose/terapia
3.
Front Immunol ; 11: 584514, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33101314

RESUMO

Physical trauma can be considered an unrecognized "pandemic" because it can occur anywhere and affect anyone and represents a global burden. Following severe tissue trauma, patients frequently develop acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) despite modern surgical and intensive care concepts. The underlying complex pathophysiology of life-threatening ALI/ARDS has been intensively studied in experimental and clinical settings. However, currently, the coronavirus family has become the focus of ALI/ARDS research because it represents an emerging global public health threat. The clinical presentation of the infection is highly heterogeneous, varying from a lack of symptoms to multiple organ dysfunction and mortality. In a particular subset of patients, the primary infection progresses rapidly to ALI and ARDS. The pathophysiological mechanisms triggering and driving severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced ALI/ARDS are still poorly understood. Although it is also generally unknown whether insights from trauma-induced ARDS may be readily translated to SARS-CoV-2-associated ARDS, it was still recommended to treat coronavirus-positive patients with ALI/ARDS with standard protocols for ALI/ARDS. However, this strategy was questioned by clinical scientists, because it was documented that some severely hypoxic SARS-CoV-2-infected patients exhibited a normal respiratory system compliance, a phenomenon rarely observed in ARDS patients with another underlying etiology. Therefore, coronavirus-induced ARDS was defined as a specific ARDS phenotype, which accordingly requires an adjusted therapeutic approach. These suggestions reflect previous attempts of classifying ARDS into different phenotypes that might overall facilitate ARDS diagnosis and treatment. Based on the clinical data from ARDS patients, two major phenotypes have been proposed: hyper- and hypo-inflammatory. Here, we provide a comparative review of the pathophysiological pathway of trauma-/hemorrhagic shock-induced ARDS and coronavirus-induced ARDS, with an emphasis on the crucial key points in the pathogenesis of both these ARDS forms. Therefore, the manifold available data on trauma-/hemorrhagic shock-induced ARDS may help to better understand coronavirus-induced ARDS.


Assuntos
Lesão Pulmonar Aguda/patologia , Infecções por Coronavirus/patologia , Pneumonia Viral/patologia , Síndrome Respiratória Aguda Grave/patologia , Trombose/patologia , Lesão Pulmonar Aguda/virologia , Betacoronavirus , Infecções por Coronavirus/tratamento farmacológico , Citocinas/sangue , Humanos , Imunidade Inata/imunologia , Inflamação/patologia , Inflamação/virologia , Pulmão/patologia , Pandemias , Pneumonia Viral/tratamento farmacológico , Síndrome Respiratória Aguda Grave/tratamento farmacológico , Síndrome Respiratória Aguda Grave/virologia , Trombose/virologia
4.
Science ; 370(6513)2020 10 09.
Artigo em Inglês | MEDLINE | ID: mdl-33033192

RESUMO

The variable outcome of viral exposure is only partially explained by known factors. We administered respiratory syncytial virus (RSV) to 58 volunteers, of whom 57% became infected. Mucosal neutrophil activation before exposure was highly predictive of symptomatic RSV disease. This was associated with a rapid, presymptomatic decline in mucosal interleukin-17A (IL-17A) and other mediators. Conversely, those who resisted infection showed presymptomatic activation of IL-17- and tumor necrosis factor-related pathways. Vulnerability to infection was not associated with baseline microbiome but was reproduced in mice by preinfection chemokine-driven airway recruitment of neutrophils, which caused enhanced disease mediated by pulmonary CD8+ T cell infiltration. Thus, mucosal neutrophilic inflammation at the time of RSV exposure enhances susceptibility, revealing dynamic, time-dependent local immune responses before symptom onset and explaining the as-yet unpredictable outcomes of pathogen exposure.


Assuntos
Mucosa Nasal/imunologia , Mucosa Nasal/virologia , Ativação de Neutrófilo , Neutrófilos/imunologia , Infecções por Vírus Respiratório Sincicial/imunologia , Vírus Sinciciais Respiratórios , Adolescente , Adulto , Animais , Contagem de Linfócito CD4 , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Quimiocina CXCL1/farmacologia , Humanos , Inflamação/imunologia , Inflamação/virologia , Interleucina-17/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Pessoa de Meia-Idade , Mucosa Nasal/patologia , Neutrófilos/efeitos dos fármacos , Infecções por Vírus Respiratório Sincicial/patologia , Fator de Necrose Tumoral alfa/imunologia , Adulto Jovem
7.
Anesth Analg ; 131(5): 1324-1333, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-33079850

RESUMO

Patients with coronavirus disease 2019 (COVID-19) frequently experience a coagulopathy associated with a high incidence of thrombotic events leading to poor outcomes. Here, biomarkers of coagulation (such as D-dimer, fibrinogen, platelet count), inflammation (such as interleukin-6), and immunity (such as lymphocyte count) as well as clinical scoring systems (such as sequential organ failure assessment [SOFA], International Society on Thrombosis and Hemostasis disseminated intravascular coagulation [ISTH DIC], and sepsis-induced coagulopathy [SIC] score) can be helpful in predicting clinical course, need for hospital resources (such as intensive care unit [ICU] beds, intubation and ventilator therapy, and extracorporeal membrane oxygenation [ECMO]) and patient's outcome in patients with COVID-19. However, therapeutic options are actually limited to unspecific supportive therapy. Whether viscoelastic testing can provide additional value in predicting clinical course, need for hospital resources and patient's outcome or in guiding anticoagulation in COVID-19-associated coagulopathy is still incompletely understood and currently under investigation (eg, in the rotational thromboelastometry analysis and standard coagulation tests in hospitalized patients with COVID-19 [ROHOCO] study). This article summarizes what we know already about COVID-19-associated coagulopathy and-perhaps even more importantly-characterizes important knowledge gaps.


Assuntos
Anti-Inflamatórios/uso terapêutico , Anticoagulantes/uso terapêutico , Betacoronavirus/patogenicidade , Coagulação Sanguínea/efeitos dos fármacos , Infecções por Coronavirus/terapia , Inflamação/terapia , Pneumonia Viral/terapia , Embolia Pulmonar/terapia , Tromboembolia Venosa/terapia , Trombose Venosa/terapia , Anti-Inflamatórios/efeitos adversos , Anticoagulantes/efeitos adversos , Biomarcadores/sangue , Infecções por Coronavirus/sangue , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/virologia , Medicina Baseada em Evidências , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Mortalidade Hospitalar , Interações Hospedeiro-Patógeno , Humanos , Inflamação/sangue , Inflamação/mortalidade , Inflamação/virologia , Mediadores da Inflamação/sangue , Pandemias , Pneumonia Viral/sangue , Pneumonia Viral/mortalidade , Pneumonia Viral/virologia , Prognóstico , Embolia Pulmonar/sangue , Embolia Pulmonar/mortalidade , Embolia Pulmonar/virologia , Fatores de Risco , Tromboembolia Venosa/sangue , Tromboembolia Venosa/mortalidade , Tromboembolia Venosa/virologia , Trombose Venosa/sangue , Trombose Venosa/mortalidade , Trombose Venosa/virologia
8.
Nat Commun ; 11(1): 5493, 2020 10 30.
Artigo em Inglês | MEDLINE | ID: mdl-33127906

RESUMO

The relationship between SARS-CoV-2 viral load and risk of disease progression remains largely undefined in coronavirus disease 2019 (COVID-19). Here, we quantify SARS-CoV-2 viral load from participants with a diverse range of COVID-19 disease severity, including those requiring hospitalization, outpatients with mild disease, and individuals with resolved infection. We detected SARS-CoV-2 plasma RNA in 27% of hospitalized participants, and 13% of outpatients diagnosed with COVID-19. Amongst the participants hospitalized with COVID-19, we report that a higher prevalence of detectable SARS-CoV-2 plasma viral load is associated with worse respiratory disease severity, lower absolute lymphocyte counts, and increased markers of inflammation, including C-reactive protein and IL-6. SARS-CoV-2 viral loads, especially plasma viremia, are associated with increased risk of mortality. Our data show that SARS-CoV-2 viral loads may aid in the risk stratification of patients with COVID-19, and therefore its role in disease pathogenesis should be further explored.


Assuntos
Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/virologia , Pneumonia Viral/virologia , Adulto , Idoso , Anticorpos Antivirais/sangue , Betacoronavirus/genética , Betacoronavirus/crescimento & desenvolvimento , Biomarcadores/sangue , Proteína C-Reativa , Infecções por Coronavirus/sangue , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/patologia , Feminino , Hospitalização , Humanos , Inflamação/sangue , Inflamação/virologia , Interleucina-6/sangue , Estudos Longitudinais , Massachusetts/epidemiologia , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/sangue , Pneumonia Viral/mortalidade , Pneumonia Viral/patologia , RNA Viral/sangue , Índice de Gravidade de Doença , Carga Viral , Viremia/sangue , Viremia/virologia
9.
Life Sci ; 261: 118355, 2020 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-32871183

RESUMO

AIMS: This study aims to cast light on immunocytometric alterations in COVID-19, a potentially fatal viral infection with heterogeneous clinical expression and a not completely defined pathophysiology. METHODS: We studied 35 COVID patients at hospital admission testing by cytofluorimetry a large panel of lymphocyte subpopulations and serum tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-17A and the soluble receptor of IL-17A (IL-17RA). KEY FINDINGS: At hospital admission, total lymphocytes and most T and B subpopulations were reduced in 50-80% of patients, with close relationship to disease severity. While activated T helper 1 (TH1) and TH17 cells resulted normal or higher. Serum IL-6 was increased in all patients, while TNF-α and IL-17A were higher in advanced stages. A patient subset with low severity had very high IL-17RA levels. Tocilizumab treatment caused an increase of IL-17A in 3/6 patients and a reduction in 3 others, while the lymphocyte number increased in 3 patients and did not change in the others. SIGNIFICANCE: Cytofluorimetry revealed a functional exhaustion of most lymphocyte populations in COVID patients not involving activated TH1 and TH17. Consequently, there was a relevant cytokines production that contributes to impair the respiratory inflammation. The increase of TH17 and IL-17 in a subset of cases and the evidence of a significant increase of IL-17RA (that prevents the interaction of IL-17 with the cell receptor) in patients with low severity suggest that some patients could benefit from monoclonal antibodies treatment targeting IL-17 pathway. Immunocytofluorimetric markers may contribute to a personalized therapy in COVID patients.


Assuntos
Infecções por Coronavirus/imunologia , Citocinas/sangue , Citometria de Fluxo/métodos , Subpopulações de Linfócitos/imunologia , Pneumonia Viral/imunologia , Idoso , Anticorpos Monoclonais Humanizados/administração & dosagem , Anticorpos Monoclonais Humanizados/farmacologia , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/virologia , Feminino , Humanos , Inflamação/imunologia , Inflamação/virologia , Contagem de Linfócitos , Masculino , Pessoa de Meia-Idade , Pandemias , Admissão do Paciente , Pneumonia Viral/fisiopatologia , Pneumonia Viral/virologia , Medicina de Precisão , Estudos Prospectivos , Índice de Gravidade de Doença
11.
J Clin Invest ; 130(11): 5674-5676, 2020 11 02.
Artigo em Inglês | MEDLINE | ID: mdl-32925166

RESUMO

In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.


Assuntos
Betacoronavirus/metabolismo , Ativação do Complemento/efeitos dos fármacos , Infecções por Coronavirus , Pandemias , Peptídeos Cíclicos/farmacologia , Pneumonia Viral , Tromboplastina/biossíntese , Microangiopatias Trombóticas , Plaquetas/metabolismo , Plaquetas/patologia , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/metabolismo , Infecções por Coronavirus/patologia , Humanos , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Inflamação/patologia , Inflamação/virologia , Neutrófilos/metabolismo , Neutrófilos/patologia , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/metabolismo , Pneumonia Viral/patologia , Índice de Gravidade de Doença , Microangiopatias Trombóticas/tratamento farmacológico , Microangiopatias Trombóticas/metabolismo , Microangiopatias Trombóticas/patologia , Microangiopatias Trombóticas/virologia
12.
Am J Trop Med Hyg ; 103(5): 1783-1796, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32940201

RESUMO

COVID-19 manifestations in symptomatic patients can be in the form of pneumonia, acute respiratory syndrome, and multiple organ dysfunction as well. Renal complications, gastrointestinal dysfunctions, endocrine system disorders, myocardial dysfunction and arrhythmia, neurological dysfunctions, dermatological symptoms, hematological manifestations, and thromboinflammation are among the reported extrapulmonary complications. Moreover, the presence of coagulopathy, excessive and dysregulated immune responses, and autoimmunity by COVID-19 patients is considerable. The pathogenesis of infection entails the entry of the virus via receptors on cells, principally angiotensin-converting enzyme 2 receptors. Direct virus damage coupled with indirect effects of viral infection including thromboinflammation, dysfunction of the immune system, and dysregulation of the renin-angiotensin system leads to multiple organ failure. This review outlines the extrapulmonary organ-specific complications and their pathophysiology and epidemiology.


Assuntos
Infecções por Coronavirus/complicações , Sistema Imunitário/fisiopatologia , Pneumonia Viral/complicações , Sistema Renina-Angiotensina , Betacoronavirus/patogenicidade , Humanos , Sistema Imunitário/virologia , Inflamação/fisiopatologia , Inflamação/virologia , Pandemias , Peptidil Dipeptidase A
13.
Endocrinology ; 161(11)2020 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-32880654

RESUMO

The coronavirus disease 2019 (COVID-19) pandemic has forced us to consider the physiologic role of obesity in the response to infectious disease. There are significant disparities in morbidity and mortality by sex, weight, and diabetes status. Numerous endocrine changes might drive these varied responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, including hormone and immune mediators, hyperglycemia, leukocyte responses, cytokine secretion, and tissue dysfunction. Studies of patients with severe COVID-19 disease have revealed the importance of innate immune responses in driving immunopathology and tissue injury. In this review we will describe the impact of the metabolically induced inflammation (meta-inflammation) that characterizes obesity on innate immunity. We consider that obesity-driven dysregulation of innate immune responses may drive organ injury in the development of severe COVID-19 and impair viral clearance.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Inflamação/imunologia , Obesidade/imunologia , Pneumonia Viral/imunologia , Betacoronavirus/fisiologia , Peso Corporal/imunologia , Infecções por Coronavirus/metabolismo , Infecções por Coronavirus/virologia , Interações Hospedeiro-Patógeno/imunologia , Humanos , Imunidade Inata/imunologia , Inflamação/metabolismo , Inflamação/virologia , Obesidade/metabolismo , Obesidade/virologia , Pandemias , Pneumonia Viral/metabolismo , Pneumonia Viral/virologia , Índice de Gravidade de Doença
15.
BMJ Case Rep ; 13(9)2020 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-32928824

RESUMO

COVID-19 is the infectious disease caused by a recently discovered SARS-CoV-2. Following an initial outbreak in December 2019 in Wuhan, China, the virus has spread globally culminating in the WHO declaring a pandemic on 11 March 2020. We present the case of a patient with an initial presentation of COVID-19 pneumonitis requiring mechanical ventilation for nearly 2 weeks and total admission time of 3 weeks. She was given prophylactic dose anticoagulation according to hospital protocol during this time. Following a week at home, she was readmitted with acute massive pulmonary embolism with severe respiratory and cardiac failure, representing the first such case in the literature.


Assuntos
Anticoagulantes/uso terapêutico , Infecções por Coronavirus/complicações , Inflamação/virologia , Pneumonia Viral/complicações , Embolia Pulmonar/virologia , Trombose/tratamento farmacológico , Trombose/virologia , Feminino , Humanos , Pessoa de Meia-Idade , Pandemias , Índice de Gravidade de Doença
16.
ASN Neuro ; 12: 1759091420954960, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32878468

RESUMO

With confirmed coronavirus disease 2019 (COVID-19) cases surpassing the 18 million mark around the globe, there is an imperative need to gain comprehensive understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the main clinical manifestations of COVID-19 are associated with respiratory or intestinal symptoms, reports of neurological signs and symptoms are increasing. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the central nervous system (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier. Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS rennin-angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for Middle East respiratory syndrome coronavirus (MERS-CoV). Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes, and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to disbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this comprehensive review, we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV; explore the potential role for astrocytes and microglia in the infection and neuroinflammation; and compare them with the previously described human and animal CoV that showed neurotropism to propose possible underlying mechanisms.


Assuntos
Astrócitos/virologia , Betacoronavirus , Sistema Nervoso Central/virologia , Infecções por Coronavirus , Microglia/virologia , Pandemias , Pneumonia Viral , Animais , Humanos , Inflamação/virologia , Coronavírus da Síndrome Respiratória do Oriente Médio , Vírus da SARS
18.
Rev Peru Med Exp Salud Publica ; 37(2): 302-311, 2020.
Artigo em Espanhol | MEDLINE | ID: mdl-32876222

RESUMO

During the first weeks of 2020, cases of SARS-CoV-2 began to be reported outside of China, with a rapid increase in cases and deaths worldwide. SARS-CoV-2 is a positive single-stranded RNA virus, encased in a lipid bilayer derived from the host cell membrane and consists of four structural proteins (S, M, E and N), plus a haemagglutinin-sterase. The binding of the S protein to the ECA2 receptor allows the entry of the virus into the host cell and is a potential therapeutic target. 81% of patients develop mild symptoms, 14% have severe symptoms and 5% require intensive care management. Fever is the most frequent symptom, followed by cough and dyspnea. Most patients do not present leukocytosis, but they do present lymphopenia with sputum cultures that do not show other pathogens. In lung biopsies of severe patients, the most noticeable finding is diffuse alveolar damage. Radiologically, ground glass and alveolar patterns are observed; the lesions being predominantly basal, subpleural, and posterior, with a multifocal peripheral distribution, more affecting the right lower lobe. There is a marked inflammatory response, up to the cytokine storm, in which anti-inflammatory treatment with pulse therapy with methylprednisolone would be indicated. Although there are no large-scale studies regarding the use of chloroquine / hydroxychloroquine, due to the global situation, its use has been authorized for its anti-SARS-CoV-2 and anti-inflammatory effect, which can be potentiated with the use of azithromycin.


Assuntos
Infecções por Coronavirus/epidemiologia , Inflamação/virologia , Pneumonia Viral/epidemiologia , Anti-Inflamatórios/administração & dosagem , Antivirais/administração & dosagem , Cloroquina/administração & dosagem , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/fisiopatologia , Humanos , Hidroxicloroquina/administração & dosagem , Inflamação/tratamento farmacológico , Pandemias , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/fisiopatologia
20.
J Clin Virol ; 131: 104611, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32882666

RESUMO

BACKGROUND: The involvement of SARS-CoV-2 antibodies in mediating immunopathogenetic events in COVID-19 patients has been suggested. By using several experimental approaches, we investigated the potential association between SARS-CoV-2 IgGs recognizing the spike (S) protein receptor-binding domain (RBD), neutralizing antibodies (NtAb) targeting S, and COVID-19 severity. PATIENTS AND METHODS: This unicenter, retrospective, observational study included 51 hospitalized patients (24 at the intensive care unit; ICU). A total of 93 sera from these patients collected at different time points from the onset of symptoms were analyzed. SARS-CoV-2 RBD IgGs were quantitated by ELISA and NtAb50 titers were measured in a GFP reporterbased pseudotyped virus platform. Demographic and clinical data, complete blood counts, as well as serum levels of ferritin, Dimer-D, C reactive protein (CRP), lactose dehydrogenase (LDH), and interleukin-6 (IL-6) were retrieved from clinical charts. RESULTS: The overall correlation between levels of both antibody measurements was good (Rho = 0.82; P = 0 < 0.001). SARS-CoV-2 RBD IgG and NtAb50 levels in sera collected up to day 30 after the onset of symptoms were comparable between ICU and non-ICU patients (P=>0.1). Four ICU patients died; two of these achieved NtAb50 titers ≥1/160 while the other two exhibited a 1/80 titer. Very weak (Rho=>0.0-<0.2) or weak (Rho=>0.2-<0.4) correlations were observed between anti-RBD IgGs, NtAb50, and serum levels pro-inflammatory biomarkers. CONCLUSIONS: The data presented herein do not support an association between SARS-CoV-2 RBD IgG or NtAb50 levels and COVID-19 severity.


Assuntos
Anticorpos Antivirais/sangue , Infecções por Coronavirus/sangue , Hospitalização/estatística & dados numéricos , Inflamação/sangue , Pneumonia Viral/sangue , Adulto , Idoso , Anticorpos Neutralizantes/sangue , Betacoronavirus , Sítios de Ligação de Anticorpos , Biomarcadores/sangue , Infecções por Coronavirus/imunologia , Feminino , Humanos , Inflamação/virologia , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/imunologia , Estudos Retrospectivos , Índice de Gravidade de Doença , Glicoproteína da Espícula de Coronavírus/imunologia , Adulto Jovem
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