FATORES IMUNOLÓGICOS E GENÉTICOS NA COVID-19
Journal: Unesc em Revista (Vol.4, No. 2)Publication Date: 2021-03-05
Authors : Linda Christian Carrijo-Carvalho; Lucas Cardoso Gobbi; Victoria Ferrari Paiva; Barbara Binow Demuner; Fábio Ramos de Souza Carvalho;
Page : 185-200
Keywords : Coronavirus; SARS-CoV-2; immunity; immune response; cross-immunity; genetic polymorphism.;
Abstract
Infection by the SARS-CoV-2 virus occurs through binding of virus S protein to the angiotensin-converting enzyme 2 (ECA2), which acts as a receptor for the virus in human cells. The new coronavirus is the causative agent of COVID-19, with different clinical conditions and, in the most severe cases, can be fatal. The wide individual variability in the manifestation of the disease has motivated discussions in the medical and academic community about the factors that influence the susceptibility of individuals to infection and the worsening of the disease. This article consists of a search carried out in databases of indexed articles, seeking to relate individual genetic characteristics and immune response to the pathophysiology of COVID-19. Different clinical presentations of COVID-19 were observed, ranging from asymptomatic individuals or those with mild illness to severe or critical conditions. It was also observed the report of individuals resistant to infection, even when exposed to the virus. The individual variability observed may be the result of genetic polymorphisms associated with expression of ECA2 or innate immunity errors. Cross-immunity may also be a factor that influences susceptibility to SARS-CoV-2 infection providing a certain degree of protection. Individuals previously exposed to other outbreak-causing coronaviruses (SARS-CoV-1 and MERS-CoV) or coronavirus associated to common colds may present antibodies and T-lymphocytes with cross-reactivity to the new coronavirus. On the other hand, the exacerbation of the immune response is considered an aggravating factor of disease, since the intense production of cytokines and the tissue damage resulting from the inflammatory response are part of the mechanisms in the pathophysiology of COVID-19.
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