The release of membrane-bound vesicles from cells is being increasingly recognized as a mechanism of intercellular communication. Extracellular vesicles (EVs) or exosomes are produced by virus-infected cells and are thought to be involved in intercellular communication between infected and uninfected cells. Viruses, in particular oncogenic viruses and viruses that establish chronic infections, have been shown to modulate the production and content of EVs. Viral microRNAs, proteins and even entire virions can be incorporated into EVs, which can affect the immune recognition of viruses or modulate neighbouring cells. Researchers from the University of North Carolina at Chapel Hill discuss the roles that EVs have during viral infection to either promote or restrict viral replication in target cells. They also discuss our current understanding of the molecular mechanisms that underlie these roles, the potential consequences for the infected host and possible future diagnostic applications.
The main vesicular egress pathways of a cell
The late endosome or multivesicular body (MVB) sorts contents from the early endosome into either the lysosome or extracellular vesicles (EVs) for egress. The early endosome is the first step in vesicle uptake and recycling. The highlighted proteins and complexes have demonstrated functions in the biogenesis of EVs or virus maturation. CCV, clathrin-coated vesicle; ER, endoplasmic reticulum; ESCRT, endosomal sorting complex required for transport; EXPH5, exophilin 5; LAMP1, lysosome-associated membrane glycoprotein 1; SYTL4, synaptotagmin-like protein 4.