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3.
Pan Afr Med J ; 36: 167, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32952811

RESUMO

Coronavirus disease 2019 (COVID-19) has been reported as the possible cause of acute myocarditis. Myocarditis is an inflammatory heart disease mostly caused by viral infections. Cytomegalovirus (CMV) primary infection is often not suspected as a cause of myocarditis in immune-competent adults. We report the case of a 37-year-old male admitted with fever, cough and dyspnea. Chest CT showed typical ground-glass changes indicative of viral pneumonia. He was tested negative for COVID-19 but had biological markers that made us still suspect it. He had elevated troponin I level (up to 111.5 ng/mL) and diffuse myocardial dyskinesia along with a decreased left ventricular ejection fraction (LVEF). He was diagnosed with CMV myocarditis with cardiac insufficiency and totally recovered without antiviral therapy. During the COVID-19 pandemic patients may develop myocarditis, still every myocarditis is not a COVID infection. Myocarditis linked to CMV infection may be rare, but life-threatening.


Assuntos
Infecções por Coronavirus/diagnóstico , Infecções por Citomegalovirus/diagnóstico , Miocardite/diagnóstico , Pneumonia Viral/diagnóstico , Técnicas de Laboratório Clínico , Infecções por Coronavirus/epidemiologia , Tosse/etiologia , Infecções por Citomegalovirus/virologia , Diagnóstico Diferencial , Dispneia/etiologia , Febre/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Miocardite/diagnóstico por imagem , Miocardite/virologia , Pandemias , Pneumonia Viral/epidemiologia , Tomografia Computadorizada por Raios X
4.
BMJ Case Rep ; 13(9)2020 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-32928810

RESUMO

Myocarditis is well known to be caused by viral infections such as Coxsackie virus group B, human herpes virus 6 and parvovirus B19. However, during the current emerging outbreak of SARS-CoV-2, there have been few case reports describing myocarditis as a possible presentation. In our case report we describe, early cardiac manifestations of SARS-CoV-2 in a UK District General Hospital. A 44-year-old Caucasian woman without any comorbidities presented with SARS-CoV-2 related fulminant myocarditis without initial respiratory symptoms. Patient underwent treatment with milrinone and methylprednisolone that showed reduction in myocardial inflammation and significantly improved myocardial contractility. This was then followed by a second phase of SARS-CoV-2 associated pneumonia and renal failure requiring ventilatory support and haemofiltration. Although, not described in the literature, we have found conjunctive use of milrinone and methylprednisolone effective in patient with SARS-CoV-2 fulminant myocarditis.


Assuntos
Infecções por Coronavirus/diagnóstico , Miocardite/virologia , Pneumonia Viral/diagnóstico , Adulto , Feminino , Humanos , Pandemias , Fatores de Tempo
5.
Cardiol Rev ; 28(6): 308-311, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32941261

RESUMO

Cardiac involvement as a complication of severe acute respiratory syndrome coronavirus 2 infection in children is a relatively new entity. We present our initial experience managing children with coronavirus disease 2019-related acute myocardial injury. The 3 patients presented here represent a spectrum of the cardiac involvement noted in children with coronavirus disease 2019-related multisystem inflammatory syndrome, including myocarditis presenting as cardiogenic shock or heart failure with biventricular dysfunction, valvulitis, coronary artery changes, and pericardial effusion.


Assuntos
Betacoronavirus , Infecções por Coronavirus , Insuficiência Cardíaca , Doenças das Valvas Cardíacas , Miocardite , Pandemias , Administração dos Cuidados ao Paciente/métodos , Derrame Pericárdico , Pneumonia Viral , Síndrome de Resposta Inflamatória Sistêmica , Adolescente , Betacoronavirus/isolamento & purificação , Betacoronavirus/patogenicidade , Técnicas de Imagem Cardíaca/métodos , Criança , Pré-Escolar , Vasos Coronários/diagnóstico por imagem , Vasos Coronários/patologia , Infecções por Coronavirus/diagnóstico , Infecções por Coronavirus/fisiopatologia , Infecções por Coronavirus/terapia , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/terapia , Doenças das Valvas Cardíacas/diagnóstico , Doenças das Valvas Cardíacas/virologia , Humanos , Miocardite/terapia , Miocardite/virologia , Derrame Pericárdico/terapia , Derrame Pericárdico/virologia , Pneumonia Viral/diagnóstico , Pneumonia Viral/fisiopatologia , Pneumonia Viral/terapia , Choque Cardiogênico/etiologia , Choque Cardiogênico/terapia , Síndrome de Resposta Inflamatória Sistêmica/diagnóstico , Síndrome de Resposta Inflamatória Sistêmica/fisiopatologia , Síndrome de Resposta Inflamatória Sistêmica/terapia , Resultado do Tratamento
6.
BMJ Case Rep ; 13(8)2020 Aug 19.
Artigo em Inglês | MEDLINE | ID: mdl-32816835

RESUMO

The COVID-19 pandemic with its severe respiratory disease has caused overflow to hospitals and intensive care units. Elevated troponins and natriuretic peptides are related to cardiac injury and poor prognosis. We present a young woman with COVID-19 infection with haemodynamic instability caused by acute perimyocarditis and cardiac tamponade. Troponin T was modestly elevated. Focused cardiac ultrasound made the diagnosis. Echocardiography revealed transient thickening of the myocardial walls. After pericardial drainage and supportive care, she improved significantly within 1 week without targeted therapy. The case illustrates the importance of cardiac diagnostic imaging in patients with COVID-19 and elevated cardiac biomarkers.


Assuntos
Betacoronavirus , Tamponamento Cardíaco/virologia , Infecções por Coronavirus/complicações , Miocardite/virologia , Pneumonia Viral/complicações , Doença Aguda , Biomarcadores/sangue , Tamponamento Cardíaco/sangue , Infecções por Coronavirus/sangue , Infecções por Coronavirus/virologia , Feminino , Humanos , Pessoa de Meia-Idade , Miocardite/sangue , Pandemias , Pneumonia Viral/sangue , Pneumonia Viral/virologia , Troponina T/sangue
7.
Cochrane Database Syst Rev ; 8: CD004370, 2020 08 19.
Artigo em Inglês | MEDLINE | ID: mdl-32835416

RESUMO

BACKGROUND: This is an update of a previous review. Case reports and case series have described dramatic responses to intravenous immunoglobulin (IVIG) in people with presumed viral myocarditis, and its administration has become commonplace. OBJECTIVES: The primary objective of this review was to compare event-free (death, requirement for a cardiac transplant, or placement of a left ventricular assist device) or overall (death) survival of adults and children with presumed viral myocarditis treated with IVIG versus those who did not receive IVIG. A secondary objective was to determine if a group of patients with presumed viral myocarditis could be identified (on the basis of age, duration of symptoms, acuity of onset of symptoms, cardiac function at presentation, virological results, or the presence or absence of histological evidence of acute myocarditis on cardiac biopsy in patients in whom a biopsy was performed) who would be the most likely to benefit from IVIG. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase, DARE, CINAHL, Web of Science Core Collection, and LILACS in July 2019, and two trial registries in November 2019. We contacted authors of trials and checked reference lists of relevant papers. We applied no language restrictions. SELECTION CRITERIA: We included studies if (1) participants had a clinical diagnosis of acute myocarditis with a left ventricular ejection fraction (LVEF) ≤ 0.45, left ventricular end-diastolic diameter (LVEDD) > 2 standard deviations (SDs) above the norm, or a left ventricular shortening fraction (LVSF) > 2 SDs below the mean, with duration of cardiac symptoms < 6 months; (2) participants had no evidence of non-infectious or bacterial cardiac disease; and (3) participants were randomly assigned to receive at least 1 g/kg of IVIG versus no IVIG or placebo. We excluded studies if (1) participants had received immunosuppression before outcome assessment; or (2) onset of myocarditis was reported to have occurred < 6 months postpartum. DATA COLLECTION AND ANALYSIS: Two review authors independently screened the search results and extracted data. We assessed risk of bias with the Cochrane 'Risk of bias' tool. We conducted meta-analysis for two outcomes (overall survival and improvement in LVEF) with two adult trials. Other meta-analyses were not possible because only three relevant trials were included, and researchers analysed markedly different populations and used different outcome measures. MAIN RESULTS: In this update we added two trials to the two previously included trials. A quasi-randomised trial was previously included due to a paucity of evidence from randomised trials; however, with the addition of two new randomised trials, it was removed from this update. For two adult trials, the overall risk of bias was unclear with very low-certainty evidence for all outcomes. The first trial studied 62 adults with recent-onset dilated cardiomyopathy randomly assigned to receive IVIG or an equivalent volume of 0.1% albumin in a blinded fashion. The effect on event-free survival between groups was uncertain (risk ratio (RR) of any event 1.76, 95% confidence interval (CI) 0.48 to 6.40). The second trial studied 41 adults with acute myocarditis randomised to either high-dose IVIG (1 to 2 g/kg over two days) or no treatment. The IVIG group reported greater survival time after 60 days (no raw data, P < 0.01), but the evidence is uncertain. We pooled the reported number of deaths in both trials, with no evidence of a difference between groups (RR 0.91, 95% CI 0.23 to 3.62, I2 = 31%, very low-certainty evidence). The evidence on the effect of IVIG treatment on LVEF (pooled mean difference (MD) -0.01, 95% CI -0.06 to 0.05) after 12 months and an unknown time frame is uncertain. The results for functional capacity, assessed by peak oxygen consumption at 12 months, were uncertain (MD -0.80, 95% CI -4.57 to 2.97). The results for infusion-related side effects were also uncertain due to a very large CI (RR 20.29, 95% CI 1.25 to 329.93). Lastly, there was uncertain evidence addressing failure to attain complete recovery (RR 0.46, 95% CI 0.19 to 1.14).  Evidence for improvement in LVEDD, left ventricular shortening fraction, and hospitalisation status in adults was not reported.  In the single included paediatric trial, the overall risk of bias was low with very low-certainty evidence for all outcomes. The trial included 86 children in Egypt presenting with acute myocarditis. Children were randomly assigned to 1 g/kg IVIG daily for two consecutive days or placebo followed by echocardiography one and six months post randomisation for recording of LVEDD and LVSF. The evidence for overall survival after six months was uncertain (risk of death RR 0.48, 95% CI 0.20 to 1.15). The evidence was also uncertain for improvement in LVEDD and LVSF after six months (LVEDD MD -4.00, 95% CI -9.52 to 1.52; LVSF no raw data).  Evidence for improvement in LVEF, functional capacity, side effects, complete recovery, and hospitalisation status in children was not reported.  AUTHORS' CONCLUSIONS: Evidence from two trials of very low certainty and with unclear risk of bias provides contradictory evidence on the use of IVIG in the treatment of adults with presumed viral myocarditis. One trial reported that use of IVIG results in longer survival time after 60 days, whilst the other trial found that IVIG does not provide an appreciable benefit. The evidence of a difference in event-free or overall survival, LVEDD, or LVSF is of very low certainty in a single paediatric trial with a low risk of bias. Until higher-quality studies with low risk of bias and larger sample sizes have demonstrated benefit in a particular group of patients, the evidence for treatment with IVIG for presumed viral myocarditis is uncertain. Further studies of the pathophysiology of myocarditis would lead to improved diagnostic criteria, which would facilitate future research.


Assuntos
Imunoglobulinas Intravenosas/uso terapêutico , Miocardite/terapia , Viroses/terapia , Doença Aguda , Adulto , Viés , Criança , Humanos , Miocardite/mortalidade , Miocardite/virologia , Intervalo Livre de Progressão , Ensaios Clínicos Controlados Aleatórios como Assunto , Volume Sistólico/efeitos dos fármacos , Viroses/mortalidade
8.
Epidemiol Infect ; 148: e189, 2020 08 26.
Artigo em Inglês | MEDLINE | ID: mdl-32843127

RESUMO

Despite SARS-CoV-19 infection has a stereotypical clinical picture, isolated cases with unusual manifestations have been reported, some of them being well-known to be triggered by viral infections. However, the real frequency in COVID-19 is unknown. Analysing data of 63 822 COVID patients attending 50 Spanish emergency department (ED) during the COVID outbreak, before hospitalisation, we report frequencies of (myo)pericarditis (0.71‰), meningoencephalitis (0.25‰), Guillain-Barré syndrome (0.13‰), acute pancreatitis (0.71‰) and spontaneous pneumothorax (0.57‰). Compared with general ED population, COVID patients developed more frequently Guillain-Barré syndrome (odds ratio (OR) 4.55, 95% confidence interval (CI) 2.09-9.90), spontaneous pneumothorax (OR 1.98, 95% CI 1.40-2.79) and (myo)pericarditis (OR 1.45, 95% CI 1.07-1.97), but less frequently pancreatitis (OR 0.44, 95% CI 0.33-0.60).


Assuntos
Infecções por Coronavirus/complicações , Síndrome de Guillain-Barré/complicações , Miocardite/complicações , Pancreatite/complicações , Pericardite/complicações , Pneumonia Viral/complicações , Pneumotórax/complicações , Betacoronavirus , Síndrome de Guillain-Barré/virologia , Humanos , Miocardite/virologia , Pancreatite/virologia , Pandemias , Pericardite/virologia , Pneumotórax/virologia , Espanha/epidemiologia
10.
Cardiovasc Pathol ; 49: 107261, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32771878

RESUMO

Cardiac inflammation in Coxsackievirus B3 (CVB3)-induced myocarditis is a consequence of viral-related cardiac injury and immune response. Caspase-associated recruitment domain 9 (CARD9) is a critical adaptor protein involved in transduction of signals from various innate pattern recognition receptors. In this study, the role of CARD9 in acute viral myocarditis was evaluated. CARD9-/- and C57BL/6 mice were infected with CVB3. On day 7 postinfection, myocardial tissue and blood samples were collected and examined. After CARD9 knockout, mRNA and protein levels of transforming growth factor-ß(TGF-ß), interleukin-17A(IL-17A), and CARD domain of B-cell CLL/lymphoma 10(BCL-10) in the myocardium were markedly lower in CARD9-/- mice than in C57BL/6 mice with CVB3-induced viral myocarditis. This trend was similar for the pathological scores for inflammation and serum levels of cytokines interleukin-6(IL-6), interleukin-10(IL-10), interferon -γ(IFN-γ), TGF-ß, and IL-17A. These results suggest that the CARD9-mediated secretion of pro-inflammatory cytokines plays an important role in the immune response to acute viral myocarditis.


Assuntos
Proteínas Adaptadoras de Sinalização CARD/metabolismo , Infecções por Coxsackievirus/metabolismo , Enterovirus Humano B/imunologia , Miocardite/metabolismo , Miocárdio/metabolismo , Linfócitos T/metabolismo , Animais , Proteínas Adaptadoras de Sinalização CARD/deficiência , Proteínas Adaptadoras de Sinalização CARD/genética , Infecções por Coxsackievirus/genética , Infecções por Coxsackievirus/imunologia , Infecções por Coxsackievirus/virologia , Citocinas/genética , Citocinas/metabolismo , Modelos Animais de Doenças , Interações Hospedeiro-Patógeno , Mediadores da Inflamação/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Knockout , Miocardite/genética , Miocardite/imunologia , Miocardite/virologia , Miocárdio/imunologia , Miocárdio/patologia , Transdução de Sinais , Linfócitos T/imunologia , Linfócitos T/virologia
12.
Mol Immunol ; 124: 218-228, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32615275

RESUMO

Autoreactive T cells may contribute to post-viral myocarditis induced with Coxsackievirus B3 (CVB3), but the underlying mechanisms of their generation are unclear. Here, we have comprehensively analyzed the generation of antigen-specific, autoreactive T cells in the mouse model of CVB3 infection for antigens implicated in patients with myocarditis/dilated cardiomyopathy. First, comparative analysis of CVB3 proteome with five autoantigens led us to identify three mimicry epitopes, one each from adenine nucleotide translocator 1 (ANT), sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) and cardiac troponin I. None of these induced cross-reactive T cell responses. Next, we generated major histocompatibility complex (MHC) class II dextramers to enumerate the frequencies of antigen-specific T cells to determine whether T cells with multiple antigen specificities are generated by CVB3 infection. These analyses revealed appearance of CD4 T cells positive for SERCA2a 971-990, and cardiac myosin heavy chain-α (Myhc) 334-352 dextramers, both in the periphery and also in the hearts of CVB3-infected animals. While ANT 21-40 dextramer+ T cells were inconsistently detected, the ß1-adrenergic receptor 181-200/211-230 or branched chain α-ketoacid dehydrogenase kinase 111-130 dextramer+ cells were absent. Interestingly, SERCA2a 971-990, Myhc 334-352 and ANT 21-40 dextramer+ cells were also detected in the liver indicating that they may have a pathogenic role. Finally, we demonstrate that the SERCA2a 971-990-reactive T cells generated in CVB3 infection could transfer disease to naïve mice. The data suggest that CVB3 infection can lead to the generation of autoreactive T cells for multiple antigens indicating a possibility that the autoreactive T cells localized in the liver can potentially circulate and contribute to the development of viral myocarditis.


Assuntos
Autoantígenos/imunologia , Linfócitos T CD4-Positivos/imunologia , Infecções por Coxsackievirus/imunologia , Miocardite/imunologia , Miocardite/virologia , Animais , Autoimunidade/imunologia , Reações Cruzadas , Modelos Animais de Doenças , Enterovirus Humano B , Feminino , Masculino , Camundongos
15.
Adv Exp Med Biol ; 1207: 229-235, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32671752

RESUMO

Direct damage and immune responses after viral infection lead to myocarditis. Autophagy is involved in both viral clearance and replication. In this chapter, we will briefly describe the role of autophagy in viral myocarditis. In addition, we will discuss the role of autophagy in dilated cardiomyopathy, hypertrophic cardiomyopathy, and diabetic cardiomyopathy.


Assuntos
Autofagia , Cardiomiopatias , Miocardite , Cardiomiopatia Dilatada , Cardiomiopatia Hipertrófica , Cardiomiopatias Diabéticas , Humanos , Miocardite/complicações , Miocardite/virologia , Viroses/complicações
16.
Cardiovasc Pathol ; 49: 107260, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32683240

RESUMO

PURPOSE: to study the effect of immunosupressive therapy (IST) in the virus-negative and virus-positive patients with immune-mediated myocarditis. METHODS: in 60 patients (45 male, 46.7 ± 11.8 years, mean LV EDD, 6.7 ± 0.7 cm, EF 26.2 ± 9.1%) active/borderline myocarditis was verified by endomyocardial biopsy (n = 38), intraoperative biopsy (n = 10), examination of explanted heart (n = 3) and autopsy (n = 9). Indications for IST determined based on histological, immune activity. The follow-up was 19.0 [7.25; 40.25] months. RESULTS: The viral genome in the myocardium was detected in 32 patients (V+ group), incl. parvovirus B19 in 23. The anti-heart antibody level was equally high in the V+ and V- patients. Antiviral therapy was administered in 24 patients. IST (in 22 V+ and 24 V- patients) include steroids (n = 40), hydroxychloroquine (n = 20), azathioprine (n = 21). The significant decrease of LV EDD (6.7 ± 0.7 to 6.4 ± 0.8), PAP (48.9 ± 15.5 to 39.4 ± 11.5 mm Hg, р<0,01), increase of EF (26.5 ± 0.9 to 36.0 ± 10.8), and lower lethality (23.9% and 64.3%; RR 0.37, 95% CI 0.19-0.71), p<0.01, were found only in IST group. Significant improvement due to IST were achieved not only in V-, but also in V+ patients. CONCLUSIONS: IST in patients with immune-mediated lymphocytic myocarditis is effective and is associated with lower lethality both in virus-negative and virus-positive patients.


Assuntos
Antivirais/uso terapêutico , Autoanticorpos/sangue , Imunossupressores/uso terapêutico , Linfócitos/efeitos dos fármacos , Miocardite/tratamento farmacológico , Miocárdio/imunologia , Viroses/tratamento farmacológico , Vírus/efeitos dos fármacos , Adulto , Idoso , Biópsia , Feminino , Interações Hospedeiro-Patógeno , Humanos , Linfócitos/imunologia , Linfócitos/patologia , Linfócitos/virologia , Masculino , Pessoa de Meia-Idade , Miocardite/imunologia , Miocardite/patologia , Miocardite/virologia , Miocárdio/patologia , Resultado do Tratamento , Viroses/imunologia , Viroses/patologia , Viroses/virologia , Vírus/imunologia , Adulto Jovem
17.
Can J Cardiol ; 36(8): 1326.e5-1326.e7, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32522523
19.
Heart ; 106(15): 1127-1131, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32499236

RESUMO

The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.


Assuntos
Infecções por Coronavirus/virologia , Inflamação/virologia , Miocardite/virologia , Pneumonia Viral/virologia , Troponina/sangue , Betacoronavirus , Biomarcadores/sangue , Infecções por Coronavirus/epidemiologia , Humanos , Pandemias , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/epidemiologia , Sistema Renina-Angiotensina/fisiologia
20.
Leukemia ; 34(7): 1726-1729, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32483300

RESUMO

The scientific community faces an unexpected and urgent challenge related to the SARS-CoV-2 pandemic and is investigating the role of receptors involved in entry of this virus into cells as well as pathomechanisms leading to a cytokine "storm," which in many cases ends in severe acute respiratory syndrome, fulminant myocarditis and kidney injury. An important question is if it may also damage hematopoietic stem progenitor cells?


Assuntos
Infecções por Coronavirus/epidemiologia , Síndrome da Liberação de Citocina/epidemiologia , Células-Tronco Hematopoéticas/virologia , Inflamassomos/imunologia , Pandemias , Pneumonia Viral/epidemiologia , Síndrome Respiratória Aguda Grave/epidemiologia , Lesão Renal Aguda/epidemiologia , Lesão Renal Aguda/imunologia , Lesão Renal Aguda/prevenção & controle , Lesão Renal Aguda/virologia , Betacoronavirus/efeitos dos fármacos , Betacoronavirus/imunologia , Betacoronavirus/patogenicidade , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/virologia , Síndrome da Liberação de Citocina/imunologia , Síndrome da Liberação de Citocina/prevenção & controle , Síndrome da Liberação de Citocina/virologia , Citocinas/antagonistas & inibidores , Citocinas/genética , Citocinas/imunologia , Furanos/farmacologia , Regulação da Expressão Gênica , Células-Tronco Hematopoéticas/efeitos dos fármacos , Células-Tronco Hematopoéticas/imunologia , Humanos , Imunidade Inata/efeitos dos fármacos , Fatores Imunológicos/farmacologia , Inflamassomos/antagonistas & inibidores , Inflamassomos/genética , Miocardite/epidemiologia , Miocardite/imunologia , Miocardite/prevenção & controle , Miocardite/virologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/antagonistas & inibidores , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Proteína 3 que Contém Domínio de Pirina da Família NLR/imunologia , Peptidil Dipeptidase A/genética , Peptidil Dipeptidase A/imunologia , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/imunologia , Pneumonia Viral/virologia , Piroptose/efeitos dos fármacos , Piroptose/genética , Piroptose/imunologia , Fatores de Risco , Síndrome Respiratória Aguda Grave/imunologia , Síndrome Respiratória Aguda Grave/prevenção & controle , Síndrome Respiratória Aguda Grave/virologia , Glicoproteína da Espícula de Coronavírus/genética , Glicoproteína da Espícula de Coronavírus/imunologia , Sulfonamidas/farmacologia , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Linfócitos T/virologia
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