Change of Antigenic Determinants of SARS-CoV-2 Virus S-Protein as a Possible Cause of Antibody-Dependent Enhancement of Virus Infection and Cytokine Storm

A hypothesis is proposed that the cytokine storm syndrome, which complicates COVID-19 in some patients, is a consequence of antibody-dependent enhancement of virus infection, which is in turn happens due to a change in dominant antigenic determinants of SARS-CoV-2 S-protein. The antibody-dependent e...

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Bibliographic Details
Published in:Biophysics (Oxford) 2020, Vol.65 (4), p.703-709
Main Authors: Nechipurenko, Yu. D., Anashkina, A. A., Matveeva, O. V.
Format: Article
Language:English
Subjects:
Affinity
Antibodies
Antigenic determinants
Biological and Medical Physics
Biophysics
Cell death
Coronaviruses
COVID-19
Cytokine storm
Cytokines
Discussions
Hypotheses
Infections
Physics
Physics and Astronomy
Proteins
Severe acute respiratory syndrome coronavirus 2
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Summary:A hypothesis is proposed that the cytokine storm syndrome, which complicates COVID-19 in some patients, is a consequence of antibody-dependent enhancement of virus infection, which is in turn happens due to a change in dominant antigenic determinants of SARS-CoV-2 S-protein. The antibody-dependent enhancement of virus infection is a phenomenon in which virus-specific antibodies that are not neutralizing enhance the entry of infectious virus into immune cells causing their death. Antibody-dependent enhancement has been reported for different coronaviruses. This phenomenon happens due to a decrease in the binding strength of neutralizing antibodies to the virus, which converts these antibodies into suboptimal—not neutralizing ones. According to our hypothesis, such a decrease in affinity may be associated with a change in the conformation of the viral S-protein. We believe that this conformational change is the major factor in the switching of antibodies affinity, which triggers antibody-dependent enhancement. However, other factors that contribute to antigen drift and antigenic determinant changes may also play a role.
ISSN:0006-3509
1555-6654
DOI:10.1134/S0006350920040119