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

Abstract

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)3 and predict, using no free parameters, how the new mutations can further enhance infectiousness.