Computer models predict that Omicron may evolve into increased transmission and immune escape.
0lead researcher on the project. The Omicron variant of the coronavirus is suspected to be the most infectious yet by binding to human receptors better than the Delta variant. The yet-to-be peer-reviewed research posted on the preprint repository bioRxiv found that Omicron may have the potential to continue to evolve even stronger binding to increase transmission and infectivity. The spike protein of the coronavirus binds to a receptor on the host cells the researcher said. The study found that Omicron’s spike proteins bind better than the Delta variant to the human ACE2 receptor. However " he said. The model predicts what mutations allow better binding to host receptors and better evasion of antibodies and provide insights into future variants of concern before they emerge. The team used the model to develop an initial set of predictions about the role of mutations on infectivity and immune response evasion of Omicron and other SARS-CoV-2 variants with human host cells. "We find that Omicron has not reached its full potential to bind human host cells " said Momeni. "The modelling shows that Omicron binds to receptor proteins stronger than the Delta variant and several mutations in previous variants of concern have been shown to be important for increasing the spike's binding to human ACE2. "We use a fully quantum mechanical model to theoretically assess how different mutations in the spike can contribute to its increased Momeni said. Such mutations can be detrimental to its binding to the host receptor and were followed by additional compensatory mutations to recover the researchers said. Such mutations can potentially lead to a future variant of concern according to researchers. The scientists from Boston College in the US developed a computer model that can predict mutations in the SARS-CoV-2 virus not all mutations in the spike protein's targeting system -- known as a receptor binding domain -- are beneficial for binding. This suggests factors other than binding may also be involved in determining how the variant evolves. One possible explanation is that the variant has acquired mutations to evade host antibodies