Viral effects on the content and function of extracellular vesicles

Abstract

The release of membrane-bound vesicles from cells has been increasingly recognized as a mechanism for intercellular communication. Extracellular vesicles (EVs) are also 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, protein and even entire virions can be incorporated into EVs, which can impact immune recognition of viruses or modulate neighboring cells. In this Review, we will discuss the roles that EVs have during virus infection to either promote or restrict viral infection in target cells. We will also discuss our current understanding of the molecular mechanisms that underlie these effects, the potential consequences for the infected host, and possible future diagnostic applications.

JC Virus infected choroid plexus epithelial cells produce extracellular vesicles that infect glial cells independently of the virus attachment receptor

“…Once in the brain vesicles likely play a fundamental role in transmitting the infection to other glial cells and perhaps also to neurons in the case of granule cell neuronopathy, a rare complication of JCPyV infection of the brain [43]. Extracellular vesicles are also known to carry an abundance of regulatory molecules including transcription factors and microRNAs that influence the microenvironment of target tissues [44][45][46][47][48][49][50]. The contents of EV derived from JCPyV infected CPE cells, kidney tubule epithelial cells, and primary glial cells has yet to be examined in vitro or in vivo but such studies are likely to shed significant light on the pathogenic mechanisms of JCPyV induced disease.…”

Proteomics Analysis of Brain Tissue in a Rat Model of Ischemic Stroke in the Acute Phase

“…The extracellular membrane vesicles, including FN1, MAPK1, and PSDP, promote the therapeutic effects on brain repair as specialized cargoes of the stem cell secretome (Kim et al, 2012;Drago et al, 2013;Bruntz et al, 2014). Moreover, exsomes may induce different physiological and pathophysiological processes in a host through mediated communication (Boelens et al, 2014;Schorey et al, 2015;Zappulli et al, 2016;Raab-Traub and Dittmer, 2017;Huang and Deng, 2019). For example, damaged nerve tissues including microglia and astrocytes have been shown to release exosome, which carried inflammatory factors such as interleukin 1 to increase extracellular ATP (Fauré et al, 2006).…”

Modularized Extracellular Vesicles: The Dawn of Prospective Personalized and Precision Medicine

“…1, 2, 3 According to their subcellular origin, EVs can be mainly classified into two categories: microvesicles (MVs, also known as ectosomes or microparticles, 100–1000 nm in diameter), which are released after formation by budding from the cytomembrane, and exosomes (Exos, 30–100 nm in diameter), which are produced inside multivesicular bodies (MVBs) and released after fusion of the MVBs with the cytomembrane 4, 5, 6. In addition, apoptotic bodies (800–5000 nm in diameter), which are shed into the extracellular environment from apoptotic cells, have several characteristics in common with MVs but are rarely involved in intracellular communication compared to MVs 4.…”