Добірка наукової літератури з теми "Covid-19 – Physiopathologie"

L’émergence récente d’un nouveau coronavirus, le SARS-CoV-2, responsable de la maladie appelée COVID-19, est un nouvel avertissement du risque pour la santé publique représenté par les zoonoses virales et notamment par les coronavirus. Principalement connus pour leur capacité à infecter les voies respiratoires supérieures et inférieures, les coronavirus peuvent également affecter le système nerveux central et périphérique, comme c’est le cas pour de nombreux virus respiratoires, tels que les virus influenza ou le virus respiratoire syncytial. Les infections du système nerveux sont un problème important de santé publique car elles peuvent provoquer des atteintes dévastatrices allant jusqu’au décès du patient, en particulier lorsqu’elles surviennent chez les personnes fragilisées ou âgées plus sensibles à ce type d’infection. Les connaissances de la physiopathologie des infections par les coronavirus émergents (MERS-CoV, SARS-CoV et SARS-CoV-2) et leurs moyens d’accéder au système nerveux central sont, pour l’heure, très sommaires. Les travaux en cours visent notamment à mieux appréhender les mécanismes associés aux atteintes neurologiques observées. Dans cette revue nous aborderons l’état des connaissances actuelles sur le neurotropisme des coronavirus humains et les mécanismes associés en développant tout particulièrement les dernières données concernant le SARS-CoV-2.

Les progrès réalisés dans la compréhension de la physiopathologique de l'infection par le SRAS-CoV-2 ont démontré que les formes graves de la COVID-19 avec des dommages cellulaires importants sont dues à une libération excessive des cytokines comme l’IL-6, IL-2, l’IL-7, l’IL-10 et le TNF-alpha. De ce fait le contrôle de cette tempête cytokinique a été proposé comme un moyen de sauvetage. De multiples essais cliniques utilisant des biothérapies visant à neutraliser ces cytokines sont en cours avec des résultats prometteurs pour certains d’entre eux. Malheureusement, aucun traitement efficace que ce soit curatif ou préventif (vaccin) n’a encore vu le jour et ce malgré les efforts déployés par la communauté scientifique de par le monde depuis le début de cette pandémie.

The worldwide health catastrophe caused by the Coronavirus Disease 2019 (COVID-19) pandemic has startled world health experts. Obesity and poor physical activity levels were shown to be elevated risk factors for COVID-19 affection and physiopathology, indicating that the COVID-19 lockdown encouraged harmful dietary changes and increases in body weight in the community. Furthermore, malnutrition and deficiencies in vitamin C, D, B12, selenium, iron, omega-3, and medium and long-chain fatty acids were found in hospitalized COVID-19 patients, emphasizing the potential health benefits of vitamin C and D treatments. More research is needed to determine the full function and consequences of diet in the prevention and treatment of COVID-19 infected individuals.

The pandemic caused by the new coronavirus has sparked discussions among health professionals about the role of food and nutrition in the infectious condition caused by the SARS-CoV-2 virus in different population groups. Malnutrition, including obesity, may reflect more severe outcomes in the physiopathology of infection and systemic responses caused by COVID-19. The present work aims to make considerations directed to the nutritionist about the susceptibility of COVID-19 in individuals submitted to malnutrition, highlighting possible outcomes of the disease and the importance of nutritional care in maintaining the health of these patients. Therefore, maintaining a good nutritional status of these patients, combined with an adequate level of micronutrients will not guarantee protection against infection caused by COVID-19, however, it is essential to minimize the risks of worsening this disease.

SUMMARY INTRODUCTION A covid-19 pandemic decreed by WHO has raised greater awareness of it. EPIDEMIOLOGY The infection reached the mark of 350,000 patients in 33 countries and affected as comorbidities the presence of comorbidities and advanced age. TRANSMISSIBILITY The transmissibility calculated so far is similar to the H1N1 epidemic, but with lower mortality rates. PHYSIOPATHOLOGY The SARS-CoV-2 virus, of the Coronaviridae family, has the capacity for cellular invasion through the angiotensin-converting enzyme 2 does not have a lower respiratory epithelium and in the cells of the small intestine mucosa. CLINICAL MANIFESTATIONS a presentation can be divided into mild (fever, fatigue, cough, myalgia, and sputum) and severe (cyanosis, dyspnoea, tachypnea, chest pain, hypoxemia and need for clinical measurement) and has an estimated estimate of 2%. DIAGNOSIS allows the detection of viral load in CRP-TR of patients with high clinical suspicion. TREATMENT based on supportive measures and infection control. In severe cases, the use of medications such as hydroxychloroquine and azithromycin or medication can be promising. Take care to avoid the use of corticosteroids. There are no restrictions on the use of resources and ACEIs / ARBs.

Les infections virales respiratoires demeurent un enjeu majeur de santé publique dans le monde entier. C’est notamment le cas de la grippe, causée par les virus influenza, et de la COVID-19, une maladie infectieuse émergente due au virus SARS-CoV-2. De manière notable, les populations les plus à risque de développer des formes sévères de grippe ou de COVID-19, sont les individus obèses et les personnes âgées. Bien que l’obésité et le vieillissement soient associées à des altérations fonctionnelles majeures du tissu adipeux blanc, la participation de ce dernier dans la physiopathologie de la grippe ou de la COVID-19 reste très peu étudiée. Le projet de thèse s’inscrit dans cette thématique générale.Les travaux récents de notre équipe ont montré, chez la souris, que l’infection par le virus influenza entraine une reprogrammation métabolique des dépôts sous-cutanés de tissu adipeux blanc, notamment caractérisée par le brunissement du tissu : un phénomène qui correspond à l’émergence d’adipocytes beiges présentant une activité thermogénique accrue. Lors de ma thèse, par des approches expérimentales in vivo, in vitro, ex vivo et in silico complémentaires, nous avons montré que la réponse au stress du réticulum endoplasmique induit par l’infection par le virus de la grippe, et plus spécifiquement la voie signalétique PERK, est impliquée dans le brunissement du tissu adipeux blanc. Outre identifier un nouveau mécanisme moléculaire de régulation de la thermogenèse, nos travaux précisent un peu plus la place du tissu adipeux blanc dans l’infection grippale.En parallèle, nous avons étudié l’impact de l’infection par le virus SARS-CoV-2 sur les tissus adipeux blancs de hamsters jeunes adultes ou âgés - un modèle préclinique de COVID-19 récemment mis en place dans notre équipe. Nos résultats montrent que l’infection est plus sévère, en termes de morbi-mortalité, chez les animaux âgés que chez les jeunes adultes. L’analyse histomorphométrique des tissus adipeux blancs sous-cutanés et viscéraux a permis de montrer que l’infection par SARS-CoV-2 est associée à une diminution de la taille des adipocytes dans ces deux dépôts ; effet qui persiste uniquement chez les animaux âgés. De manière très intéressante, l’analyse histologique des tissus révèle la présence de nombreuses et larges zones de nécrose adipocytaire (ressemblant aux crown-like structures décrites dans les tissus adipeux blancs en contexte d’obésité) uniquement dans les dépôts sous-cutanés de tissu adipeux des animaux âgés, y compris à distance de l’infection. En cela, notre étude confirme et renforce les plus récentes données de la littérature qui décrivent un rôle majeur du tissu adipeux blanc dans la physiopathologie de la COVID-19
Respiratory viral infections remain a major public health issue, worldwide. This is particularly the case with flu, caused by influenza viruses, and COVID-19, an emerging infectious disease caused by the SARS-CoV-2 virus. Importantly, the populations most at risk of developing severe forms of flu or COVID-19 are obese individuals and the elderly. Although obesity and aging are both associated with major functional alterations of the white adipose tissue, the latter's involvement in the pathophysiology of influenza or COVID-19 remains poorly studied. The thesis project falls within this general theme.Recent work by our team has shown, in mice, that infection with the influenza virus causes metabolic reprogramming of the subcutaneous fat depots, mainly characterized by the browning of the tissue: a phenomenon which corresponds to the emergence of beige adipocytes with increased thermogenic activity. During my PhD, using complementary experimental in vivo, in vitro, ex vivo and in silico approaches, we showed that the response to influenza-infection-induced endoplasmic reticulum stress, and more specifically the PERK signaling pathway, is involved in white adipose tissue browning. Besides identifying a novel molecular mechanism that regulates thermogenesis, our work further specifies the role of the white adipose tissue in influenza infection.In parallel, we studied the impact of infection with the SARS-CoV-2 virus on the white adipose tissues of young adult and old hamsters - a preclinical model of COVID-19 recently implemented in our team. Our results showed that the infection is more severe - in terms of morbidity and mortality - in older animals than in young adults. Histomorphometric analysis of subcutaneous and visceral white adipose tissues showed that infection with SARS-CoV-2 is associated with a decrease in the size of adipocytes in these two depots; an effect that persists only in the older animals. Remarkably, the histological analysis of the tissues reveals the presence of numerous and large areas of adipocyte necrosis (resembling the “crown-like structures” that can be observed in white adipose tissues in the context of obesity) only in the subcutaneous fat depots of the older animals, even at distance from infection. As such, our study confirms and strengthens the most recent data in the literature, which describes a major role of the white adipose tissue in the pathophysiology of COVID-19

The past two years were deeply marked by the emergence of a global pandemic caused by the worldwide spread of the virus severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection. The plethora of repercussions on the health of those affected is extensive, ranging from asymptomatic individuals, mild flu-like disease, and severe respiratory failure, eventually leading to death. Despite this predilection for the respiratory system, the virus is responsible for multisystemic manifestations and soon became clear that neurological involvement was a frequent issue of coronavirus disease 2019 (COVID-19). Much have been pointed out about the neurotropic nature of the virus, the ways by which it invades and targets specific structures of the central nervous system, and the physiopathology behind the neurologic manifestations associated with it (namely encephalomyelitis, Guillain-Barré syndrome, lacunar infarcts, and vascular dysfunction, just to list a few). This chapter aims to raise light about the association between COVID-19 and the mechanisms of acute symptomatic seizures, through neurotropism and neuroinvasion features of SARS-CoV-2, and to review the variety of clinical presentations reported so far.

The World Health Organization (WHO) recognized the coronavirus disease (COVID-19) as a worldwide pandemic caused by a newly discovered coronavirus responsible for Severe Acute Respiratory Syndrome (SARS-Cov2). The virus appeared in Wuhan, China in December 2019 and spread throughout the world, causing several mortality cases particularly in older people and those with chronic diseases. A body of evidence suggests a multi-target of SARS-Cov2, which may act beyond the respiratory system being responsible for other pathological complications, including the gastrointestinal tract, nervous, and the renal functions. The chapter will provide a literature review of the recent data on COVID-19 physiopathology involving in addition to the respiratory dysfunction all the potential physiological functions which could be independently and directly impaired by the SARS-Cov2.

The current outbreak of the novel coronavirus, SARS-CoV-2 (coronavirus disease 2019; previously 2019- nCoV), epi-centered in Hubei Province of the People's Republic of China, has spread to many other countries caused an extreme burden for healthcare systems globally. Coronaviruses are traditionally considered nonlethal pathogens to humans, mainly causing approximately 15% of common colds. In this century, we have encountered highly pathogenic human CoVs twice. In this chapter, the authors propose to focus the gastrointestinal physiopathology of the infection of SARS-Cov2. This chapter will develop subject like the gastrointestinal manifestations of the infection to SARS-Cov2. The second part of this chapter will develop the role of the gut microbiome in the SARS-Cov2 diseases susceptibilities. And then the authors will show the etiopathogenesis of SARS-Cov2 associated diarrhea. As reported by previous studies, the SARS-Cov virus entry into host cell is mediated by the interaction between the envelop-anchored viral spike protein and the host receptor named angiotensin-converting enzyme 2 (ACE2).

During SARS-CoV-1 and Middle East Respiratory Distress Syndrome (MERS) outbreaks it was observed a particularly elevated incidence of cardiovascular disease among patients. With COVID-19, this correlation becomes evident again. However, the cardiovascular impacts by COVID-19 pandemic are not yet well established although publications about its potential deleterious effects are constant. Thus, aimed to carry a systematic review of the literature with meta-analysis, the following question was used as a guide: what practical contributions does the scientific literature produced in the period of 2019-2020 has to offer about the impact of the COVID-19 on cardiovascular system? A systematic review of the literature using the Virtual Health Library (VHL) and PubMed with the following descriptors: #1 “cardiovascular disease” [MeSH] AND #2 “COVID-19” [keyword], as well as their equivalents in the Portuguese and Spanish language, during the period from December 2019 to March 2020 was performed. One hundred articles were found in Pubmed and twenty-seven were selected. In VHL there are 59 articles and four were selected totaling thirty-one papers. The findings were then divided into three subcategories: Etiology, Physiopathology and Risk factors of SARS-CoV-2 in Cardiovascular System; Clinical presentation, laboratory markers and imagenological aspects of SARS-CoV-2 in cardiovascular system; and Anti-Hypertensive Drugs, Cardiovascular System and SARS-CoV-2. When it comes to the cardiovascular system, these issues are aggravated and urge as a joint commitment from researchers, medical and governmental organizations to carry out more robust studies with bold methodologies aimed at mapping prognostic factors and assertive therapeutic approaches in the management of cardiovascular complications of COVID- 19.

Introdução: A doença COVID-19, causada pelo novo coronavírus SARSCoV-2 está relacionada a um amplo espectro clínico, isto é, estão presentes desde casos assintomáticos até falência de múltiplos órgãos e morte. Em estágios iniciais de doença, a frequente porta de entrada pela via inalatória nasal e inicio de comprometimento do sistema respiratório resultam em sintomas gripais, incluindo febre, tosse seca, astenia, mialgia, cefaleia, disgeusia e hiposmia/anosmia. No entanto, possivelmente devido ao tropismo do vírus pelos pneumócitos II, 20% dos pacientes evoluem rapidamente para doença grave com pneumonia intersticial, síndrome do desconforto respiratório agudo (SDRA), e outras disfunções envolvendo diferentes órgãos e sistemas. Até 80% destes pacientes evoluem ao óbito. A função imune dos hospedeiros infectados parece ser o principal determinante na apresentação e progressão da doença. Na ausência de comorbidades é frequente a resolução da infecção em estágios iniciais. Por outro lado, idade aumentada ou imunidade prejudicada, combinada com outras comorbidades como hipertensão e diabetes são fatores relacionados a formas graves de doença. Objetivos: revisar as principais características clínicas e mecanismos fisiopatológicos da doença COVID-19 por meio de revisão de literatura. Métodos: Foram Selecionados artigos bem avaliados e canalizados na temática proposta na base de dados MEDLINE/PubMed. Foram buscados artigos entre os anos de 2020 a 2022 combinando os termos MeSH: “clinical”, “COVID”, “mechanism”, “physiopathology” e “SARS-CoV-2”. A área temática do estudo é Clínica Médica. Resultados: O SARS-CoV-2 infecta células humanas ligando-se à enzima conversora de angiotensina 2 (ECA-2) através da proteína “spike” (S) de sua superfície. Esta interação é capaz de desregular o sistema renina-angiotensinaaldosterona diminuindo a conversão de angiotensina II em angiotensina 1- 7. Como resultado, ocorre aumento das vias pró-trombóticas e diminuição das vias antitrombóticas. A partir disso, inicia-se um ciclo de estado inflamatório sistêmico envolvendo inflamação (IL-1, IL-6, quimiocinas), resposta imunológica (Th1) e dano endotelial progressivo. A ativação de células endoteliais pelo Sars-CoV-2 aumenta a externalização do fator de Von Willebrand e moléculas de adesão de leucócitos ICAM-1, VCAM-1, e E selectina, permitindo a adesão de plaquetas e neutrófilos, além da expressão do fator tecidual ativando a via de coagulação extrínseca e, por sua vez, a geração de α-trombina levando à geração de fibrina e ativação de plaquetas. Desse modo, ambas vias de coagulação são ativadas. Como resultado, ocorrem complicações tais quais: tromboembolismo da artéria pulmonar, trombose venosa profunda, infarto agudo do miocárdio, acidente vascular encefálico e Coagulação Intravascular Disseminada associada ao COVID-19. Patologias relacionadas ao dano endotelial crônico como DM e HAS, e as que amplificam a inflamação (como a obesidade) são capazes de atuar sinergicamente com os diversos mecanismos mencionados. Conclusão: O estudo revisa as diversas apresentações clinicas da COVID-19 e revisita asperamente as principais complicações e um possível mecanismo fisiopatológico, demonstrando o aprendizado crescente sobre esta doença emergente e desafiadora. Por fim, reforça-se a necessidade da manutenção de pesquisas sobre a COVID-19 desde sua fisiopatologia até o desenvolvimento de intervenções eficientes para cursos de doença grave e associados a complicações. Resumo- sem apresentação oral. PALAVRAS-CHAVE: COVID-19, Inflamação, Medicina Clínica, Patologia Clínica, SARS-CoV-2