How viruses and toxins disassemble to enter host cells

Abstract

Many viruses and toxins disassemble to enter host cells and cause disease. These conformational changes must be orchestrated temporally and spatially during entry to avoid premature disassembly leading to nonproductive pathways. Although viruses and toxins are evolutionarily distinct toxic agents, emerging findings in their respective fields have revealed that the cellular locations supporting disassembly, the host factors co-opted during disassembly, the nature of the conformational changes, and the physiological function served by disassembly are strikingly conserved. Here, we examine some of the shared disassembly principles observed in model viruses and toxins. Where appropriate, we also underscore their differences. Our major intention is to draw together the fields of viral and toxin cell entry by using lessons gleaned from each field to inform and benefit one another.