What cellular mechanisms are related to thromboembolic events in patients with COVID-19?

SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. This disease is beginning to be better understood in terms of its other, non-respiratory, clinical manifestations. Over the course of months caring for patients infected by the virus, clinical and laboratory changes have been identified that have prompted researchers to debate the potential that SARS-CoV-2 has to trigger an exacerbated immune response that is capable of changing endothelial homeostasis through both direct and indirect mechanisms. With the intention of contributing to this debate, a review was conducted of the possible mechanisms that could trigger these phenomena in patients with COVID-19. It is important to understand the pathophysiology of the immunological mechanisms related to this disease in order to understand the potential endothelial damage that COVID-19 can provoke.

Quais são os mecanismos celulares relacionados aos eventos tromboembólicos em pacientes com COVID-19? / What cellular mechanisms are related to thromboembolic events in patients with COVID-19?

Resumo O SARS-CoV-2 é o vírus responsável pela pandemia da COVID-19. Essa doença começou a ser melhor entendida devido a outras manifestações clínicas além das respiratórias. Ao longo dos meses de atendimento aos pacientes infectados pelo vírus, foram identificadas alterações clínicas e laboratoriais que incitaram os pesquisadores a discutir sobre o potencial do SARS-CoV-2 no desencadeamento de uma resposta imunológica exacerbada capaz de alterar a homeostase endotelial, através de mecanismos diretos e indiretos. Com esse intuito, foram revisados os possíveis mecanismos que desencadeiam este fenômeno em pacientes portadores de COVID-19. Dessa forma, torna-se importante o entendimento fisiopatológico dos mecanismos imunológicos relacionados à doença para a compreensão do potencial de dano endotelial que a COVID-19 pode promover.

Abstract SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. This disease is beginning to be better understood in terms of its other, non-respiratory, clinical manifestations. Over the course of months caring for patients infected by the virus, clinical and laboratory changes have been identified that have prompted researchers to debate the potential that SARS-CoV-2 has to trigger an exacerbated immune response that is capable of changing endothelial homeostasis through both direct and indirect mechanisms. With the intention of contributing to this debate, a review was conducted of the possible mechanisms that could trigger these phenomena in patients with COVID-19. It is important to understand the pathophysiology of the immunological mechanisms related to this disease in order to understand the potential endothelial damage that COVID-19 can provoke.