Modelling the Interactions Between SARS-CoV-2 Spike Protein and Monoclonal Antibodies to Inform Translational Approaches to Treat COVID-19 Infection

Abstract

Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is the virus responsible for the coronavirus disease (COVID-19) pandemic. It was first detected in Wuhan, China, in late December of 2019 and, as of April 2021, has infected over 140 million people worldwide, resulting in three million deaths. Scientists across the globe have worked tirelessly over the past year and have developed four vaccines currently licenced by the European Medicines Agency. In late 2020, several variants of concern established themselves globally; including the B.1.1.7 (Alpha), B.1.351 (Beta) and P.1 (Gamma) variants which have several concerning mutations. Initial data has shown that these variants can be more infectious and even escape antibody neutralisation. This means natural immunity from past infection and even vaccination may not be enough to bring the pandemic to an end. Understanding how the virus's entry is facilitated by its spike protein is essential to testing the antibodies' efficacy and understanding the pitfalls of previous research. The knowledge gained on the importance of the variants' mutations and how they may evade antibodies are key to developing novel monoclonal antibodies (mAbs), updated vaccines, and finally the research into preventing future variants via mAb cocktails and ones that target conserved epitopes. This study explored the relationship between mAbs and the SARS-CoV-2 spike protein and how it is augmented in response to the novel variants and in what manner issues may be overcome.