Phase transitions may explain why SARS-CoV-2 spreads so fast and why new variants are spreading faster

The novel coronavirus SARS CoV-2 responsible for the COVID-19 pandemic and SARS CoV-1 responsible for the SARS epidemic of 2002-2003 share an ancestor yet evolved to have much different transmissibility and global impact¹. A previously developed thermodynamic model of protein conformations predicted that SARS CoV-2 is very close to a thermodynamic critical point, which makes it highly infectious but also easily displaced by a spike-based vaccine because there is a tradeoff between transmissibility and robustness². The model identified a small cluster of four key mutations of SARS CoV-2 that promotes much stronger viral attachment and viral spreading. Here we apply the model to two new strains (B.1.1.7 and B.1.351)³and predict, using no free parameters, how the new mutations can further enhance infectiousness.