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1.
Clin Lab ; 68(8)2022 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-35975504

RESUMO

BACKGROUND: Novel coronavirus disease 2019 (COVID-19), which has been a global pandemic for nearly 2 years, presents with highly variable clinical manifestations in both the acute and post-acute periods. This study evaluated the relationship between CRP/albumin ratio and pulmonary function at 12 weeks in patients with post-acute COVID-19. METHODS: The study included 157 patients with a previous diagnosis of COVID-19 pneumonia who presented to our outpatient clinic with symptoms of post-acute COVID-19 (12 weeks after first testing positive) between July 2021 and October 2021. Patients who had non-severe pneumonia were included in group 1, severe pneumonia that did not require intensive care in group 2, and severe pneumonia that required intensive care in group 3. RESULTS: At 12 weeks, group 3 had significantly lower percent predicted forced expiratory volume in 1 second (FEV1%), percent predicted forced vital capacity (FVC%), percent predicted diffusing capacity of the lungs for carbon monoxide (DLCO%), and oxygen saturation (SO2) compared to patients in groups 1 and 2 (p = 0.001, 0.04, 0.001, and 0.001, respectively). CRP/albumin ratio was significantly lower in group 2 compared to groups 1 and 3 (p = 0.001). Correlation analysis independent of age and comorbidity showed that CRP/albumin ratio was negatively correlated with SO2, FEV1%, FVC%, and DLCO%. CONCLUSIONS: CRP and albumin levels have prognostic significance during acute COVID-19 infection. The negative correlation between CRP/albumin ratio and respiratory function observed in our study suggest this parameter may be used in the follow-up of patients presenting at 12 weeks with post-acute COVID-19 symptoms.


Assuntos
COVID-19 , Pulmão , Albuminas/análise , Proteína C-Reativa/análise , COVID-19/complicações , COVID-19/fisiopatologia , Volume Expiratório Forçado , Humanos , Pulmão/fisiopatologia , Capacidade Vital
2.
G Ital Cardiol (Rome) ; 23(9): 651-662, 2022 Sep.
Artigo em Italiano | MEDLINE | ID: mdl-36039714

RESUMO

Recent evidence shows that a range of persistent or new symptoms can manifest after 4-12 weeks in a subset of patients who have recovered from acute SARS-CoV-2 infection, and this condition has been coined long COVID by COVID-19 survivors among social support groups. Long COVID can affect the whole spectrum of people with COVID-19, from those with very mild acute disease to the most severe forms. Like the acute form, long COVID has multisystemic aspects. Patients can manifest with a very heterogeneous multitude of symptoms, including fatigue, post-exertional malaise, dyspnea, cognitive impairment, sleep disturbances, anxiety and depression, muscle pain, brain fog, anosmia/dysgeusia, headache, and limitation of functional capacity, which impact their quality of life. Because of the extreme clinical heterogeneity, and also due to the lack of a shared, specific definition, it is very difficult to know the real prevalence and incidence of this condition. Risk factors for developing long COVID would be female sex, initial severity, and comorbidities. Globally, with the re-emergence of new waves, the population of people infected with SARS-CoV-2 continues to expand rapidly, necessitating a more thorough understanding of potential sequelae of COVID-19. This review summarizes up to date definitions and epidemiological aspects of long COVID.


Assuntos
COVID-19 , COVID-19/complicações , COVID-19/epidemiologia , COVID-19/fisiopatologia , COVID-19/psicologia , Humanos , Qualidade de Vida , Fatores de Risco , SARS-CoV-2/patogenicidade , Sobreviventes
3.
Front Cell Infect Microbiol ; 12: 896504, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35967852

RESUMO

The gut microbiome profile of COVID-19 patients was found to correlate with a viral load of SARS-CoV-2, COVID-19 severity, and dysfunctional immune responses, suggesting that gut microbiota may be involved in anti-infection. In order to investigate the role of gut microbiota in anti-infection against SARS-CoV-2, we established a high-throughput in vitro screening system for COVID-19 therapeutics by targeting the endoribonuclease (Nsp15). We also evaluated the activity inhibition of the target by substances of intestinal origin, using a mouse model in an attempt to explore the interactions between gut microbiota and SARS-CoV-2. The results unexpectedly revealed that antibiotic treatment induced the appearance of substances with Nsp15 activity inhibition in the intestine of mice. Comprehensive analysis based on functional profiling of the fecal metagenomes and endoribonuclease assay of antibiotic-enriched bacteria and metabolites demonstrated that the Nsp15 inhibitors were the primary bile acids that accumulated in the gut as a result of antibiotic-induced deficiency of bile acid metabolizing microbes. This study provides a new perspective on the development of COVID-19 therapeutics using primary bile acids.


Assuntos
Ácidos e Sais Biliares , COVID-19 , Endorribonucleases , Microbioma Gastrointestinal , SARS-CoV-2 , Proteínas não Estruturais Virais , Animais , Antibacterianos/farmacologia , Ácidos e Sais Biliares/fisiologia , COVID-19/tratamento farmacológico , COVID-19/fisiopatologia , Endorribonucleases/antagonistas & inibidores , Endorribonucleases/metabolismo , Endorribonucleases/fisiologia , Microbioma Gastrointestinal/fisiologia , Camundongos , Proteínas não Estruturais Virais/antagonistas & inibidores , Proteínas não Estruturais Virais/metabolismo , Proteínas não Estruturais Virais/fisiologia
4.
Saudi Med J ; 43(6): 579-586, 2022 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-35675937

RESUMO

OBJECTIVES: To investigate the relationship between physical activity level and disease severity, anxiety level, sleep quality, and fatigue in patients followed up with COVID-19 diagnosis. METHODS: This was a cross-sectional study of 111 volunteer patients who were receiving treatment with COVID-19 diagnosis at the Chest Diseases Polyclinic, Sanko University, Sani Konukoglu Practice and Research Hospital, Gaziantep, Turkey between May 2021 and July 2021 were included in the study and classified clinically and radiologically. They were evaluated on the basis of demographic characteristics, International Physical Activity Questionnaire, Beck Anxiety Inventory, Pittsburgh Sleep Quality Index, and Fatigue Severity Scale. RESULTS: Approximately 63% of the patients did not have a habit of exercise, while 52.3% of our patients were clinically mild cases, and 33.3% had normal lung tomography. While clinical disease severity was not associated with exercise habits, sleep quality was impaired in clinically severe patients. CONCLUSION: The results of our study suggested that physical inactivity is common. Anxiety is a frequent symptom in COVID-19 cases and also COVID-19 negatively affects sleep quality.


Assuntos
COVID-19 , Exercício Físico , Ansiedade/epidemiologia , COVID-19/diagnóstico , COVID-19/fisiopatologia , COVID-19/terapia , Estudos Transversais , Exercício Físico/fisiologia , Fadiga/epidemiologia , Seguimentos , Humanos , Índice de Gravidade de Doença , Qualidade do Sono
5.
Bol. malariol. salud ambient ; 62(1): 32-38, jun, 2022. tab, ilus
Artigo em Espanhol | LILACS, LIVECS | ID: biblio-1379293

RESUMO

Hay dos tipos principales de tejido adiposo; el subcutáneo, que es menos activo metabólicamente, y el tejido adiposo visceral, que secreta constantemente citocinas inflamatorias y está relacionado a enfermedades metabólicas y cardiovasculares. Nuestro objetivo fue identificar la asociación entre el exceso de grasa visceral y la severidad de enfermedad en pacientes con COVID-19. Se realizó un estudio observacional analítico que incluyó a pacientes con COVID-19 admitidos al Hospital Carrión de Huancayo, Perú. Se utilizó la balanza de bioimpedancia para cuantificar la composición corporal, la variable dependiente fue la severidad de enfermedad. Se utilizó el análisis de regresión logística para determinar la asociación de la grasa visceral y otros parámetros antropométricos con severidad de enfermedad. Se analizaron a 120 personas con COVID-19, la edad promedio fue 50 años, el sexo masculino fue 60%. De acuerdo a los valores de la composición corporal emitidos por el equipo de bioimpedancia: La grasa visceral > 15Kg (OR 7,31; p = 0,001); la grasa corporal total > 35% (OR 5,58; p = 0,009) y el exceso de peso > 20Kg (OR 6,96; p = 0,011) fueron los parámetros asociados a enfermedad severa por COVID-19. La relación positiva entre el perímetro abdominal y la cantidad de grasa visceral fue significativo (p = 0,01). En la composición corporal, el exceso de grasa visceral es el mayor parámetro asociado a enfermedad severa por COVID-19(AU)


There are two main types of adipose tissue; the subcutaneous, which is less metabolically active, and the visceral adipose tissue, which constantly secretes inflammatory cytokines and is related to metabolic and cardiovascular diseases. Our objetive was to identify the association between the excess of visceral fat and disease severity in COVID-19 patients. An analytical observational study was carried out which included patients with COVID-19 admitted to the Carrión Hospital in Huancayo, Peru. The bioimpedance balance was used to quantify the body composition; the dependent variable was the severity of the disease. A logistic regression analysis was used to determine the association of visceral fat and other anthropometric parameters with the severity of the disease. Out of 120 people with COVID-19 were analyzed, the average age was 50 years, the male sex was 60%. According to the body composition values issued by the bioimpedance team: Visceral fat> 15Kg (OR 7.31; p = 0.001); Total body fat> 35% (OR 5.58; p = 0.009) and excess weight> 20Kg (OR 6.96; p = 0.011) were the parameters associated with severe disease due to COVID-19. The positive relationship between abdominal circumference and the amount of visceral fat was significant (p = 0.01). In body composition, excess visceral fat is the main parameter associated with severe COVID-19 disease(AU)


Assuntos
Humanos , Masculino , Feminino , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Síndrome do Desconforto Respiratório do Recém-Nascido/epidemiologia , Gordura Intra-Abdominal/fisiopatologia , COVID-19/fisiopatologia , COVID-19/epidemiologia , Obesidade/fisiopatologia , Peru/epidemiologia , Índice de Gravidade de Doença , Índice de Massa Corporal , Modelos Logísticos , Análise de Regressão , Hospitais
6.
Nature ; 606(7915): S5-S6, 2022 06.
Artigo em Inglês | MEDLINE | ID: mdl-35732779
7.
Biosensors (Basel) ; 12(6)2022 Jun 05.
Artigo em Inglês | MEDLINE | ID: mdl-35735538

RESUMO

Biophysical insults that either reduce barrier function (COVID-19, smoke inhalation, aspiration, and inflammation) or increase mechanical stress (surfactant dysfunction) make the lung more susceptible to atelectrauma. We investigate the susceptibility and time-dependent disruption of barrier function associated with pulmonary atelectrauma of epithelial cells that occurs in acute respiratory distress syndrome (ARDS) and ventilator-induced lung injury (VILI). This in vitro study was performed using Electric Cell-substrate Impedance Sensing (ECIS) as a noninvasive evaluating technique for repetitive stress stimulus/response on monolayers of the human lung epithelial cell line NCI-H441. Atelectrauma was mimicked through recruitment/derecruitment (RD) of a semi-infinite air bubble to the fluid-occluded micro-channel. We show that a confluent monolayer with a high level of barrier function is nearly impervious to atelectrauma for hundreds of RD events. Nevertheless, barrier function is eventually diminished, and after a critical number of RD insults, the monolayer disintegrates exponentially. Confluent layers with lower initial barrier function are less resilient. These results indicate that the first line of defense from atelectrauma resides with intercellular binding. After disruption, the epithelial layer community protection is diminished and atelectrauma ensues. ECIS may provide a platform for identifying damaging stimuli, ventilation scenarios, or pharmaceuticals that can reduce susceptibility or enhance barrier-function recovery.


Assuntos
COVID-19 , Atelectasia Pulmonar/etiologia , Síndrome do Desconforto Respiratório , Lesão Pulmonar Induzida por Ventilação Mecânica , COVID-19/complicações , COVID-19/fisiopatologia , Impedância Elétrica , Humanos , Pulmão/fisiopatologia , Pneumonia Aspirativa/complicações , Pneumonia Aspirativa/fisiopatologia , Atelectasia Pulmonar/fisiopatologia , Lesão por Inalação de Fumaça/etiologia , Lesão por Inalação de Fumaça/fisiopatologia , Lesão Pulmonar Induzida por Ventilação Mecânica/complicações , Lesão Pulmonar Induzida por Ventilação Mecânica/prevenção & controle
8.
Allergy Asthma Proc ; 43(3): 187-193, 2022 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-35524358

RESUMO

Background: Long COVID (coronavirus disease 2019) syndrome includes a group of patients who, after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibit lingering mild-to-moderate symptoms and develop medical complications that can have lasting health problems. In this report, we propose a model for the pathophysiology of the long COVID presentation based on increased proinflammatory cytokine production that results from the persistence of the SARS-CoV-2 virus or one of its molecular components. Associated with this hyperproduction of inflammatory cytokines is a heightened activity of nuclear factor κ B (NF-κB) and p38 mitogen-activated protein kinase signaling pathways that regulate cytokine production. Objective: The purpose of the present report was to review the causes of long COVID syndrome and suggest ways that can provide a basis for a better understanding of the clinical symptomatology for the of improved diagnostic and therapeutic procedures for the condition. Methods: Extensive research was conducted in medical literature data bases by applying terms such as "long COVID" associated with "persistence of the SARS-CoV-2 virus" "spike protein' "COVID-19" and "biologic therapies." Results and Conclusions: In this model of the long COVID syndrome, the persistence of SARS-CoV-2 is hypothesized to trigger a dysregulated immune system with subsequent heightened release of proinflammatory cytokines that lead to chronic low-grade inflammation and multiorgan symptomatology. The condition seems to have a genetic basis, which predisposes individuals to have a diminished immunologic capacity to completely clear the virus, with residual parts of the virus persisting. This persistence of virus and resultant hyperproduction of proinflammatory cytokines are proposed to form the basis of the syndrome.


Assuntos
COVID-19 , Citocinas , COVID-19/complicações , COVID-19/fisiopatologia , Citocinas/metabolismo , Humanos , SARS-CoV-2
9.
Adv Biol (Weinh) ; 6(7): e2101327, 2022 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-35523737

RESUMO

Sars-Cov-2 may trigger molecular and functional alterations of cardiomyocytes (CMs) of the heart due to the presence of receptor angiotensin-converting enzyme 2 (ACE2) of the host cells. While the endocytic itinerary of the virus via cleavage of the spike protein of Sars-Cov-2 is well understood, the role of the remaining part of the spike protein subunit and ACE2 complex is still elusive. Herein, the possible effects of this complex are investigated by using synthetic spike proteins of Sars-Cov-2, human-induced pluripotent stem cells (hiPSC), and a culture device made of an arrayed monolayer of cross-linked nanofibers. hiPSCs are first differentiated into CMs that form cardiac tissue-like constructs with regular beating and expression of both ACE2 and gap junction protein Connexin 43. When incubated with the spike proteins, the hiPSC-CMs undergo a rhythmic fluctuation with overstretched sarcomere structures and dispersed gap junction proteins. When incubated with the spike proteins and supplementary angiotensin II, the damage of the spike protein on hiPSC-CMs is enhanced due to downregulated ACE2, chromatin margination, altered Connexin 43 expression, sarcomere disruption, and beating break. This discovery may imply latent effects of the spike proteins on the heart.


Assuntos
Enzima de Conversão de Angiotensina 2 , COVID-19 , Miócitos Cardíacos , SARS-CoV-2 , Glicoproteína da Espícula de Coronavírus , Angiotensina II/farmacologia , Enzima de Conversão de Angiotensina 2/metabolismo , COVID-19/metabolismo , COVID-19/patologia , COVID-19/fisiopatologia , Conexina 43/metabolismo , Técnicas de Cultura , Humanos , Células-Tronco Pluripotentes Induzidas , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Miócitos Cardíacos/virologia , SARS-CoV-2/metabolismo , Glicoproteína da Espícula de Coronavírus/química , Glicoproteína da Espícula de Coronavírus/metabolismo
10.
Biomed Res Int ; 2022: 8078259, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35528173

RESUMO

Coronaviruses are a family of viruses that infect mammals and birds. Coronaviruses cause infections of the respiratory system in humans, which can be minor or fatal. A comparative transcriptomic analysis has been performed to establish essential profiles of the gene expression of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) linked to cystic fibrosis (CF). Transcriptomic studies have been carried out in relation to SARS-CoV-2 since a number of people have been diagnosed with CF. The recognition of differentially expressed genes demonstrated 8 concordant genes shared between the SARS-CoV-2 and CF. Extensive gene ontology analysis and the discovery of pathway enrichment demonstrated SARS-CoV-2 response to CF. The gene ontological terms and pathway enrichment mechanisms derived from this research may affect the production of successful drugs, especially for the people with the following disorder. Identification of TF-miRNA association network reveals the interconnection between TF genes and miRNAs, which may be effective to reveal the other influenced disease that occurs for SARS-CoV-2 to CF. The enrichment of pathways reveals SARS-CoV-2-associated CF mostly engaged with the type of innate immune system, Toll-like receptor signaling pathway, pantothenate and CoA biosynthesis, allograft rejection, graft-versus-host disease, intestinal immune network for IgA production, mineral absorption, autoimmune thyroid disease, legionellosis, viral myocarditis, inflammatory bowel disease (IBD), etc. The drug compound identification demonstrates that the drug targets of IMIQUIMOD and raloxifene are the most significant with the significant hub DEGs.


Assuntos
COVID-19 , Fibrose Cística , COVID-19/genética , COVID-19/fisiopatologia , Fibrose Cística/genética , Fibrose Cística/fisiopatologia , Perfilação da Expressão Gênica , Ontologia Genética , Humanos , MicroRNAs/genética , SARS-CoV-2 , Fatores de Transcrição/genética
11.
Chin J Integr Med ; 28(7): 627-635, 2022 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-35583580

RESUMO

OBJECTIVE: To investigate how the National Health Commission of China (NHCC)-recommended Chinese medicines (CMs) modulate the major maladjustments of coronavirus disease 2019 (COVID-19), particularly the clinically observed complications and comorbidities. METHODS: By focusing on the potent targets in common with the conventional medicines, we investigated the mechanisms of 11 NHCC-recommended CMs in the modulation of the major COVID-19 pathophysiology (hyperinflammations, viral replication), complications (pain, headache) and comorbidities (hypertension, obesity, diabetes). The constituent herbs of these CMs and their chemical ingredients were from the Traditional Chinese Medicine Information Database. The experimentally-determined targets and the activity values of the chemical ingredients of these CMs were from the Natural Product Activity and Species Source Database. The approved and clinical trial drugs against these targets were searched from the Therapeutic Target Database and DrugBank Database. Pathways of the targets was obtained from Kyoto Encyclopedia of Genes and Genomes and additional literature search. RESULTS: Overall, 9 CMs modulated 6 targets discovered by the COVID-19 target discovery studies, 8 and 11 CMs modulated 8 and 6 targets of the approved or clinical trial drugs for the treatment of the major COVID-19 complications and comorbidities, respectively. CONCLUSION: The coordinated actions of each NHCC-recommended CM against a few targets of the major COVID-19 pathophysiology, complications and comorbidities, partly have common mechanisms with the conventional medicines.


Assuntos
COVID-19 , Medicina Tradicional Chinesa , COVID-19/complicações , COVID-19/tratamento farmacológico , COVID-19/epidemiologia , COVID-19/fisiopatologia , Comorbidade , Medicamentos de Ervas Chinesas/uso terapêutico , Humanos , Medicina , SARS-CoV-2
12.
J Med Virol ; 94(9): 4088-4096, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35538614

RESUMO

Innate and acquired immunity responses are crucial for viral infection elimination. However, genetic variations in coding genes may exacerbate the inflammation or initiate devastating cytokine storms which poses severe respiratory conditions in coronavirus disease-19 (COVID-19). Host genetic variations in particular those related to the immune responses determine the patients' susceptibility and COVID-19 severity and pathophysiology. Gene polymorphisms such as single nucleotide polymorphisms (SNPs) of interferons, TNF, IL1, IL4, IL6, IL7, IL10, and IL17 predispose patients to the severe form of COVID-19 or severe acute respiratory syndrome coronavirus-2 (SARS-COV-2). These variations mainly alter the gene expression and cause a severe response by B cells, T cells, monocytes, neutrophils, and natural killer cells participating in a cytokine storm. Moreover, cytokines and chemokines SNPs are associated with the severity of COVID-19 and clinical outcomes depending on the corresponding effect. Additionally, genetic variations in genes encoding toll-like receptors (TLRs) mainly TLR3, TLR7, and TLR9 have been related to the COVID-19 severe respiratory symptoms. The specific relation of these mutations with the novel variants of concern (VOCs) infection remains to be elucidated. Genetic variations mainly within genes encoding proinflammatory cytokines, cytokine receptors, and TLRs predispose patients to COVID-19 disease severity. Understanding host immune gene variations associated with the SARS-COV-2 infection opens insights to control the pathophysiology of emerging viral infections.


Assuntos
COVID-19 , Citocinas , Receptores de Citocinas , Receptores Toll-Like , COVID-19/genética , COVID-19/fisiopatologia , Síndrome da Liberação de Citocina/genética , Citocinas/genética , Humanos , Receptores de Citocinas/genética , SARS-CoV-2 , Receptores Toll-Like/genética
13.
Urologiia ; (2): 122-125, 2022 May.
Artigo em Russo | MEDLINE | ID: mdl-35485825

RESUMO

The SARS-CoV-2 pandemic has brought serious economic and social problems worldwide'. Due to its medical consequences, it is of importance to study the mechanisms of the disease and new therapeutic interventions, as well as rehabilitation processes. Despite the fact that the genome of the new coronavirus has been sequenced and studied, clinical and epidemiological data are constantly updated and analyzed, and exact pathogenesis has not yet been understood. At the same time, domestic and foreign studies suggest that the virus is an agent that affects not only the lungs, vascular wall, hemostasis, but also the reproductive system. The aim of the review is to summarize the current knowledge about novel SARS-CoV-2, including its pathophysiology and potential impact on male reproductive function.


Assuntos
COVID-19/complicações , Doenças dos Genitais Masculinos/virologia , Genitália Masculina/fisiopatologia , Genitália Masculina/virologia , SARS-CoV-2 , COVID-19/epidemiologia , COVID-19/fisiopatologia , COVID-19/virologia , Doenças dos Genitais Masculinos/epidemiologia , Doenças dos Genitais Masculinos/fisiopatologia , Humanos , Masculino , Saúde Reprodutiva , SARS-CoV-2/genética
15.
Nature ; 606(7914): 585-593, 2022 06.
Artigo em Inglês | MEDLINE | ID: mdl-35483404

RESUMO

Severe COVID-19 is characterized by persistent lung inflammation, inflammatory cytokine production, viral RNA and a sustained interferon (IFN) response, all of which are recapitulated and required for pathology in the SARS-CoV-2-infected MISTRG6-hACE2 humanized mouse model of COVID-19, which has a human immune system1-20. Blocking either viral replication with remdesivir21-23 or the downstream IFN-stimulated cascade with anti-IFNAR2 antibodies in vivo in the chronic stages of disease attenuates the overactive immune inflammatory response, especially inflammatory macrophages. Here we show that SARS-CoV-2 infection and replication in lung-resident human macrophages is a critical driver of disease. In response to infection mediated by CD16 and ACE2 receptors, human macrophages activate inflammasomes, release interleukin 1 (IL-1) and IL-18, and undergo pyroptosis, thereby contributing to the hyperinflammatory state of the lungs. Inflammasome activation and the accompanying inflammatory response are necessary for lung inflammation, as inhibition of the NLRP3 inflammasome pathway reverses chronic lung pathology. Notably, this blockade of inflammasome activation leads to the release of infectious virus by the infected macrophages. Thus, inflammasomes oppose host infection by SARS-CoV-2 through the production of inflammatory cytokines and suicide by pyroptosis to prevent a productive viral cycle.


Assuntos
COVID-19 , Inflamassomos , Macrófagos , SARS-CoV-2 , Enzima de Conversão de Angiotensina 2 , Animais , COVID-19/patologia , COVID-19/fisiopatologia , COVID-19/virologia , Humanos , Inflamassomos/metabolismo , Interleucina-1 , Interleucina-18 , Pulmão/patologia , Pulmão/virologia , Macrófagos/metabolismo , Macrófagos/patologia , Macrófagos/virologia , Camundongos , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Pneumonia/metabolismo , Pneumonia/virologia , Piroptose , Receptores de IgG , SARS-CoV-2/metabolismo , SARS-CoV-2/patogenicidade
16.
Cells ; 11(8)2022 04 11.
Artigo em Inglês | MEDLINE | ID: mdl-35455977

RESUMO

The novel coronavirus (2019-nCoVCOVID-19) belongs to the Beta coronavirus family, which contains MERS-CoV (Middle East respiratory syndrome coronavirus) and SARS-CoV (severe acute respiratory syndrome coronavirus). SARS-CoV-2 activates the innate immune system, thereby activating the inflammatory mechanism, causing the release of inflammatory cytokines. Moreover, it has been suggested that COVID-19 may penetrate the central nervous system, and release inflammatory cytokines in the brains, inducing neuroinflammation and neurodegeneration. Several links connect COVID-19 with Alzheimer's disease (AD), such as elevated oxidative stress, uncontrolled release of the inflammatory cytokines, and mitochondrial apoptosis. There are severe concerns that excessive immune cell activation in COVID-19 may aggravate the neurodegeneration and amyloid-beta pathology of AD. Here, we have collected the evidence, showing the links between the two diseases. The focus has been made to collect the information on the activation of the inflammation, its contributors, and shared therapeutic targets. Furthermore, we have given future perspectives, research gaps, and overlapping pathological bases of the two diseases. Lastly, we have given the short touch to the drugs that have equally shown rescuing effects against both diseases. Although there is limited information available regarding the exact links between COVID-19 and neuroinflammation, we have insight into the pathological contributors of the diseases. Based on the shared pathological features and therapeutic targets, we hypothesize that the activation of the immune system may induce neurological disorders by triggering oxidative stress and neuroinflammation.


Assuntos
COVID-19 , Doenças Neuroinflamatórias , Doença de Alzheimer/virologia , Antioxidantes/metabolismo , COVID-19/complicações , COVID-19/fisiopatologia , Citocinas , Humanos , Doenças Neuroinflamatórias/virologia , Estresse Oxidativo , SARS-CoV-2
17.
PLoS One ; 17(3): e0265202, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35312682

RESUMO

BACKGROUND: Non-invasive ventilation (NIV) has been increasingly used in COVID-19 patients. The limited physiological monitoring and the unavailability of respiratory mechanic measures, usually obtainable during invasive ventilation, is a limitation of NIV for ARDS and COVID-19 patients management. OBJECTIVES: This pilot study was aimed to evaluate the feasibility of non-invasively monitoring respiratory mechanics by oscillometry in COVID-19 patients with moderate-severe acute respiratory distress syndrome (ARDS) receiving NIV. METHOD: 15 COVID-19 patients affected by moderate-severe ARDS at the RICU (Respiratory Intensive Care Unit) of the University hospital of Cattinara, Trieste, Italy were recruited. Patients underwent oscillometry tests during short periods of spontaneous breathing between NIV sessions. RESULTS: Oscillometry proved to be feasible, reproducible and well-tolerated by patients. At admission, 8 of the 15 patients showed oscillometry parameters within the normal range which further slightly improved before discharge. At discharge, four patients had still abnormal respiratory mechanics, not exclusively linked to pre-existing respiratory comorbidities. Lung mechanics parameters were not correlated with oxygenation. CONCLUSIONS: Our results suggest that lung mechanics provide complementary information for improving patients phenotyping and personalisation of treatments during NIV in COVID 19 patients, especially in the presence of respiratory comorbidities where deterioration of lung mechanics may be less coupled with changes in oxygenation and more difficult to identify. Oscillometry may provide a valuable tool for monitoring lung mechanics in COVID 19 patients receiving NIV.


Assuntos
COVID-19/terapia , Pulmão/fisiopatologia , Ventilação não Invasiva/métodos , Oscilometria/métodos , Síndrome do Desconforto Respiratório/virologia , Adulto , Idoso , COVID-19/fisiopatologia , Estudos de Viabilidade , Feminino , Humanos , Itália , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Síndrome do Desconforto Respiratório/fisiopatologia , Síndrome do Desconforto Respiratório/terapia , Mecânica Respiratória , Estudos Retrospectivos
18.
Front Immunol ; 13: 821721, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35296077

RESUMO

Many studies already reported on the association between patient characteristics on the severity of COVID-19 disease outcome, but the relation with SARS-CoV-2 antibody levels is less clear. To investigate this in more detail, we performed a retrospective observational study in which we used the IgG antibody response from 11,118 longitudinal antibody measurements of 2,082 unique COVID convalescent plasma donors. COVID-19 symptoms and donor characteristics were obtained by a questionnaire. Antibody responses were modelled using a linear mixed-effects model. Our study confirms that the SARS-CoV-2 antibody response is associated with patient characteristics like body mass index and age. Antibody decay was faster in male than in female donors (average half-life of 62 versus 72 days). Most interestingly, we also found that three symptoms (headache, anosmia, nasal cold) were associated with lower peak IgG, while six other symptoms (dry cough, fatigue, diarrhoea, fever, dyspnoea, muscle weakness) were associated with higher IgG concentrations.


Assuntos
Fatores Etários , COVID-19/imunologia , COVID-19/terapia , SARS-CoV-2/fisiologia , Adulto , Anticorpos Antivirais/sangue , Formação de Anticorpos , Doadores de Sangue , Índice de Massa Corporal , COVID-19/epidemiologia , COVID-19/fisiopatologia , Convalescença , Feminino , Humanos , Imunização Passiva/métodos , Imunoglobulina G/sangue , Masculino , Pessoa de Meia-Idade , Países Baixos/epidemiologia , Estudos Retrospectivos
19.
Respir Res ; 23(1): 68, 2022 Mar 22.
Artigo em Inglês | MEDLINE | ID: mdl-35317815

RESUMO

BACKGROUND: Patient hospitalized for coronavirus disease 2019 (COVID-19) pulmonary infection can have sequelae such as impaired exercise capacity. We aimed to determine the frequency of long-term exercise capacity limitation in survivors of severe COVID-19 pulmonary infection and the factors associated with this limitation. METHODS: Patients with severe COVID-19 pulmonary infection were enrolled 3 months after hospital discharge in COVulnerability, a prospective cohort. They underwent cardiopulmonary exercise testing, pulmonary function test, echocardiography, and skeletal muscle mass evaluation. RESULTS: Among 105 patients included, 35% had a reduced exercise capacity (VO2peak < 80% of predicted). Compared to patients with a normal exercise capacity, patients with reduced exercise capacity were more often men (89.2% vs. 67.6%, p = 0.015), with diabetes (45.9% vs. 17.6%, p = 0.002) and renal dysfunction (21.6% vs. 17.6%, p = 0.006), but did not differ in terms of initial acute disease severity. An altered exercise capacity was associated with an impaired respiratory function as assessed by a decrease in forced vital capacity (p < 0.0001), FEV1 (p < 0.0001), total lung capacity (p < 0.0001) and DLCO (p = 0.015). Moreover, we uncovered a decrease of muscular mass index and grip test in the reduced exercise capacity group (p = 0.001 and p = 0.047 respectively), whilst 38.9% of patients with low exercise capacity had a sarcopenia, compared to 10.9% in those with normal exercise capacity (p = 0.001). Myocardial function was normal with similar systolic and diastolic parameters between groups whilst reduced exercise capacity was associated with a slightly shorter pulmonary acceleration time, despite no pulmonary hypertension. CONCLUSION: Three months after a severe COVID-19 pulmonary infection, more than one third of patients had an impairment of exercise capacity which was associated with a reduced pulmonary function, a reduced skeletal muscle mass and function but without any significant impairment in cardiac function.


Assuntos
COVID-19/complicações , Tolerância ao Exercício/fisiologia , Pneumonia/fisiopatologia , Idoso , COVID-19/fisiopatologia , Estudos de Coortes , Ecocardiografia/métodos , Ecocardiografia/estatística & dados numéricos , Teste de Esforço/métodos , Teste de Esforço/estatística & dados numéricos , Tolerância ao Exercício/imunologia , Feminino , Seguimentos , França , Humanos , Pulmão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Pneumonia/etiologia , Estudos Prospectivos , Testes de Função Respiratória/métodos , Testes de Função Respiratória/estatística & dados numéricos , Insuficiência Respiratória/etiologia , Insuficiência Respiratória/fisiopatologia
20.
Biomed Pharmacother ; 148: 112756, 2022 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-35228064

RESUMO

The 2019 corona virus disease (COVID-19) has caused a global chaos, where a novel Omicron variant has challenged the healthcare system, followed by which it has been referred to as a variant of concern (VOC) by the World Health Organization (WHO), owing to its alarming transmission and infectivity rate. The large number of mutations in the receptor binding domain (RBD) of the spike protein is responsible for strengthening of the spike-angiotensin-converting enzyme 2 (ACE2) interaction, thereby explaining the elevated threat. This is supplemented by enhanced resistance of the variant towards pre-existing antibodies approved for the COVID-19 therapy. The manuscript brings into light failure of existing therapies to provide the desired effect, however simultaneously discussing the novel possibilities on the verge of establishing suitable treatment portfolio. The authors entail the risks associated with omicron resistance against antibodies and vaccine ineffectiveness on one side, and novel approaches and targets - kinase inhibitors, viral protease inhibitors, phytoconstituents, entry pathways - on the other. The manuscript aims to provide a holistic picture about the Omicron variant, by providing comprehensive discussions related to multiple aspects of the mutated spike variant, which might aid the global researchers and healthcare experts in finding an optimised solution to this pandemic.


Assuntos
COVID-19/fisiopatologia , SARS-CoV-2/genética , SARS-CoV-2/metabolismo , Enzima de Conversão de Angiotensina 2/metabolismo , Animais , COVID-19/imunologia , Vacinas contra COVID-19/imunologia , Catepsinas/metabolismo , Receptores ErbB/antagonistas & inibidores , Humanos , Esquemas de Imunização , Imunização Secundária , Fitoterapia/métodos , Plantas Medicinais , Ligação Proteica/fisiologia , Domínios e Motivos de Interação entre Proteínas/fisiologia , Elementos Estruturais de Proteínas/fisiologia , Glicoproteína da Espícula de Coronavírus/metabolismo , Inibidores de Protease Viral/farmacologia , Inibidores de Protease Viral/uso terapêutico
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