Synchronized Attachment and the Darwinian Evolution of Coronaviruses CoV-1 and CoV-2

TL;DR

This paper investigates the evolutionary mechanisms behind the increased danger of CoV-2 compared to CoV-1, identifying mutations that enhance viral attachment and proposing a new infection stage based on biomolecular evolution theory.

Contribution

It introduces a novel evolutionary framework to understand coronavirus infectivity, highlighting specific mutations that improve viral attachment and suggesting new targets for vaccine development.

Findings

CoV-2 has mutations that promote stronger viral attachment.

A new infection stage precedes structural rearrangements.

Evolutionary theory explains the virus's increased contagiousness.

Abstract

CoV2019 has evolved to be much more dangerous than CoV2003. Experiments suggest that structural rearrangements dramatically enhance CoV2019 activity. We identify a new first stage of infection which precedes structural rearrangements by using biomolecular evolutionary theory to identify sequence differences enhancing viral attachment rates. We find a small cluster of mutations which show that CoV-2 has a new feature that promotes much stronger viral attachment and enhances contagiousness. The extremely dangerous dynamics of human coronavirus infection is a dramatic example of evolutionary approach of self-organized networks to criticality. It may favor a very successful vaccine. The identified mutations can be used to test the present theory experimentally.