Effect of the charge distribution of virus coat proteins on the length of packaged RNAs

TL;DR

This paper investigates how the distribution of charges on virus coat proteins influences the length of RNA packaged, revealing that both electrostatics and genome entropy jointly affect virus assembly.

Contribution

It introduces a mean-field theoretical model that accounts for charge distribution and genome entropy, advancing understanding of virus assembly mechanisms.

Findings

Electrostatics alone cannot fully explain RNA packaging.

Genome configurational entropy significantly influences RNA length.

Charge distribution on capsid proteins affects assembly outcomes.

Abstract

Single-stranded RNA viruses efficiently encapsulate their genome into a protein shell called the capsid. Electrostatic interactions between the positive charges in the capsid protein's N-terminal tail and the negatively charged genome have been postulated as the main driving force for virus assembly. Recent experimental results indicate that the N-terminal tail with the same number of charges and same lengths package different amounts of RNA, which reveals that electrostatics alone cannot explain all the observed outcomes of the RNA self-assembly experiments. Using a mean-field theory, we show that the combined effect of genome configurational entropy and electrostatics can explain to some extent the amount of packaged RNA with mutant proteins where the location and number of charges on the tails are altered. Understanding the factors contributing to the virus assembly could promote the attempt to block viral infections or to build capsids for gene therapy applications.