tetano
Editor, Senior Moderator
Life Sci
. 2021 Feb 17;119245.
doi: 10.1016/j.lfs.2021.119245. Online ahead of print.
A double edged-sword - The Complement System during SARS-CoV-2 infection
Lazara Elena Santiesteban-Lores[SUP] 1 [/SUP], Thais Akemi Amamura[SUP] 1 [/SUP], Tiago Francisco da Silva[SUP] 1 [/SUP], Leonardo Moura Midon[SUP] 1 [/SUP], Milena Carvalho Carneiro[SUP] 1 [/SUP], Lourdes Isaac[SUP] 2 [/SUP], Lorena Bavia[SUP] 3 [/SUP]
Affiliations
Abstract
In the past 20 years, infections caused by coronaviruses SARS-CoV, MERS-CoV and SARS-CoV-2 have posed a threat to public health since they may cause severe acute respiratory syndrome (SARS) in humans. The Complement System is activated during viral infection, being a central protagonist of innate and acquired immunity. Here, we report some interactions between these three coronaviruses and the Complement System, highlighting the central role of C3 with the severity of these infections. Although it can be protective, its role during coronavirus infections seems to be contradictory. For example, during SARS-CoV-2 infection, Complement System can control the viral infection in asymptomatic or mild cases; however, it can also intensify local and systemic damage in some of severe COVID-19 patients, due to its potent proinflammatory effect. In this last condition, the activation of the Complement System also amplifies the cytokine storm and the pathogenicity of coronavirus infection. Experimental treatment with Complement inhibitors has been an enthusiastic field of intense investigation in search of a promising additional therapy in severe COVID-19 patients.
Keywords: COVID-19; Complement System; Complement inhibitors; Inflammation; SARS-CoV-2.
. 2021 Feb 17;119245.
doi: 10.1016/j.lfs.2021.119245. Online ahead of print.
A double edged-sword - The Complement System during SARS-CoV-2 infection
Lazara Elena Santiesteban-Lores[SUP] 1 [/SUP], Thais Akemi Amamura[SUP] 1 [/SUP], Tiago Francisco da Silva[SUP] 1 [/SUP], Leonardo Moura Midon[SUP] 1 [/SUP], Milena Carvalho Carneiro[SUP] 1 [/SUP], Lourdes Isaac[SUP] 2 [/SUP], Lorena Bavia[SUP] 3 [/SUP]
Affiliations
- PMID: 33609539
- DOI: 10.1016/j.lfs.2021.119245
Abstract
In the past 20 years, infections caused by coronaviruses SARS-CoV, MERS-CoV and SARS-CoV-2 have posed a threat to public health since they may cause severe acute respiratory syndrome (SARS) in humans. The Complement System is activated during viral infection, being a central protagonist of innate and acquired immunity. Here, we report some interactions between these three coronaviruses and the Complement System, highlighting the central role of C3 with the severity of these infections. Although it can be protective, its role during coronavirus infections seems to be contradictory. For example, during SARS-CoV-2 infection, Complement System can control the viral infection in asymptomatic or mild cases; however, it can also intensify local and systemic damage in some of severe COVID-19 patients, due to its potent proinflammatory effect. In this last condition, the activation of the Complement System also amplifies the cytokine storm and the pathogenicity of coronavirus infection. Experimental treatment with Complement inhibitors has been an enthusiastic field of intense investigation in search of a promising additional therapy in severe COVID-19 patients.
Keywords: COVID-19; Complement System; Complement inhibitors; Inflammation; SARS-CoV-2.