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look at the C3 and C5 proteins in the Covid-19

Henry David Mosquera-Daza · Universidad de Antioquia · 2021

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The emergency caused by the new SARS-CoV-2 virus, which causes the Covid-19 disease, has triggered a global pandemic. One of the most characteristic factors of SARS-CoV-2 virus infection is the deregulated activation of the complement system, especially by proteins C3 and C5. These proteins trigger initiation reactions such as maintenance of inappropriate biological activities in addition to uncontrolled immune responses by immune cells, especially neutrophils. They generate various pathologies such as acute stroke, heart attack, coagulopathies, multiorgan failure, inflammation, immunothrombinosis, heart failure, acute kidney injury, acute injuries in the lung area, thrombotic microangiopathy, pneumonia, and dysfunctional immune responses. Because of the crucial role played by proteins C3 and C5 in the infection by the SARS-COV-2 virus, new complement system inhibition treatments have emerged as a possible first line of defense against the worst symptoms developed during Covid-19 disease. This article will review in a general way, the role of C3 and C5 proteins and the treatments aimed at the inhibition of these same proteins during SARS-CoV-2 infection.

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APA 7

Mosquera-Daza, H. D. (2021). look at the C3 and C5 proteins in the Covid-19. https://doi.org/10.17533/udea.acbi.v43n115a05

MLA

Mosquera-Daza, Henry David. "look at the C3 and C5 proteins in the Covid-19." 2021. https://doi.org/10.17533/udea.acbi.v43n115a05.

Chicago

Mosquera-Daza, Henry David. 2021. "look at the C3 and C5 proteins in the Covid-19.". https://doi.org/10.17533/udea.acbi.v43n115a05.

Harvard

Mosquera-Daza, H. D. 2021, look at the C3 and C5 proteins in the Covid-19, Universidad de Antioquia, available at: https://doi.org/10.17533/udea.acbi.v43n115a05 [Accessed 29 Jun. 2026].

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Título
look at the C3 and C5 proteins in the Covid-19
Autor / colaboradores
Henry David Mosquera-Daza
Editorial
Universidad de Antioquia
Año de publicación
2021
ISSN
2145-7166
ISSN
2145-7166
Idioma
eng

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