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Source: Antibody-Dependent Enhancement (ADE)   Sep 28, 2020  3 years, 6 months, 2 weeks, 5 days, 7 hours, 4 minutes ago

Antibody-Dependent Enhancement (ADE) Phenomenon Could Be Caused By SARS-COV-2 Antibody- Anti-N-Protein IgG, Increasing COVID-19 Severity

Antibody-Dependent Enhancement (ADE) Phenomenon Could Be Caused By SARS-COV-2 Antibody- Anti-N-Protein IgG, Increasing COVID-19 Severity
Source: Antibody-Dependent Enhancement (ADE)   Sep 28, 2020  3 years, 6 months, 2 weeks, 5 days, 7 hours, 4 minutes ago
Antibody-Dependent Enhancement (ADE): Researchers from the University of Miami, Miami VA Healthcare System and Express Gene in a news study have identified the anti-N Immunoglobulin G (IgG) antibodies against SARS-CoV-2 as possibly being the  cause of the Antibody-Dependent Enhancement (ADE) phenomenon in patients experiencing COVID-19 severity. Furthermore the same antibodies could also act as non-neutralizing antibodies to the virus so that immune cells are activated but without viral destruction. This leads to the cascading release of excessive amounts of pro-inflammatory cytokines as well as the blockade of anti-inflammatory chemicals.


 
The study findings are published in a preprint server and are pending peer review. https://www.medrxiv.org/content/10.1101/2020.09.23.20197251v1
 
The novel SARS-CoV-2 coronavirus is a single-stranded RNA virus belonging to the Betacoronavirus family that has four key structural proteins of which the nucleocapsid protein or N protein is one.
 
Although the host immune response involves immunoglobulin G (IgG) developed against the various structural proteins, the anti-spike protein IgG is thought to be primarily responsible for neutralizing immunity and is, therefore the focus of many vaccine trials for COVID-19.
 
However the N protein is currently known to be required for the structure and function of viral RNA, being involved in the transcription of viral RNA as well as for assembly of viral particles, in addition to its RNA chaperone function. It comprises three regions, one repeating sequence which determines the length of its amino acids, one sumoylation motif, and one kinase-dependent phosphorylation-determining serine residue.
 
Typically most neutralizing antibodies are known to inhibit SARS-CoV-2 infection by blocking the binding of the viral spike protein with the ACE2 receptor on the host cell.
 
Alarmingly, there are some modes of antibody action that are harmful and damaging such as the antibody-dependent enhancement (ADE) phenomenon.
 
Antibody-dependent enhancement or ADE phenomenon occurs when non-neutralizing antibody attached to immune cells called macrophages and cytotoxic T cells, hence mediating the binding of the SARS-CoV-2 coronavirus to these host cells.
 
As a result, these cells are destroyed, weakening the immune response rather than strengthening it. The outcome is increased amounts of virus in the body and bloodstream.
 
Also another harmful route of antibody action on the host cell involves the binding of non-neutralizing antibodies to the virus so that immune cells are activated but without viral destruction. This leads to the cascading release of excessive amounts of pro-inflammatory cytokines as well as the blockade of anti-inflammatory chemicals, thus leading to a destructive immunological imbalance called the cytokine storm.
 
The researchers suspect that such processes may be at work in COVID-19 due to infections by cross-reacting strains of coronavirus in the past. In fact, the N protein of SARS-CoV-2 has a high degree of homology with other virulent coronaviruses. This agrees with the concept of a high level of cross-reacting n on-neutralizing antibodies present early in the disease, leading to ADE and precipitating a ‘cytokine storm’ as well as higher levels of infection.
 
The University of Miami study sought to explore the possibility that anti-N IgG was acting in this manner, leading to ADE and increased viremia in COVID-19.
 
Hence this should then be linked to higher chances of