Modeling study suggests how different SARS-CoV-2 mutations prevent antibody binding
Using three classes of antibodies, researchers modeled their binding to the SARS-CoV-2 virus spike protein. They found binding to key residues in current mutations changes how the spike protein moves and can lead to binding resistance.
The spike protein of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) adopts several conformations when it binds to host receptors. Antibodies against the virus often compete with the host receptors to bind to the spike protein and interfere with the processes that change the spike protein conformation.
Some antibodies can bind to different parts of the spike protein simultaneously, providing a more potent neutralizing capacity. Class I antibodies have a considerable overlap with the angiotensin-converting enzyme 2 (ACE2) receptor and bind when the receptor-binding domain (RBD) is in the open or up conformation.
Speed of vaccination is key to reducing COVID-19 spread, says study
Mathematical modeling of the effects of vaccine efficacy and the speed of vaccination show that a lower efficacy vaccine may curb disease transmission similar to that of a higher efficacy vaccine if the speed of immunization is high.
To combat the COVID-19 pandemic, several vaccines have now been approved and are being administered to populations across the globe. However, one concern has been the vaccines efficacy against emerging variants of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). These vaccines were only tested on the original strain of the virus.
The spike protein is the main part of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for the infection. It consists of two subunits S1 and S2. Upon entry of the virus into the human body, the S1 subunit helps the virus bind to the angiotensin-converting enzyme 2 (ACE2) receptors on host cells.
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Oxford-AstraZeneca COVID vaccine induces cell spikes similar to SARS-CoV-2 s
Scientists from the University of Oxford and the University of Southampton report in the journal
ACS Central Science that cells infected with the ChAdOx1 vaccine produce spike proteins on the cells similar to those produced by natural SARS-CoV-2 infection.
Artist imaging of protein spike on the surface of cells exposed to the vaccine. Image Credit: University of Southampton
The spike protein of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which protrudes from the virus envelope, is the key structure responsible for infecting host cells. The S1 subunit helps bind the virus to the angiotensin-converting enzyme 2 (ACE2), and the S2 subunit helps with membrane fusion with the host cell.