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 impact(1). A previously developed thermodynamic model of protein conformations hypothesized that SARS CoV-2 is very close to a new 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 robustness(2). The model identified a small cluster of four key mutations of SARS CoV-2 that predicts much stronger viral attachment and viral spreading compared to SARS CoV-1. Here we apply the model to the SARS-CoV-2 variants Alpha (B.1.1.7), Beta (B.1.351), Gamma (P.1) and Delta (B.1.617.2)(3) and predict, using no free parameters, how the new mutations will not diminish the effectiveness of current spike based vaccines and may even further enhance infectiousness by augmenting the binding ability of the virus. Published by Elsevier B.V.

Automated summary

This study predicts the transmissibility and vaccine effectiveness of the novel coronavirus SARS-CoV-2 and its variants using a thermodynamic model of protein conformations. The findings suggest that the mutations in SARS-CoV-2 and its variants will not diminish the efficacy of spike-based vaccines and may even enhance viral infectivity.