Skip to main content
. Author manuscript; available in PMC: 2016 Oct 1.
Published in final edited form as: Virology. 2015 Jul 1;484:288–304. doi: 10.1016/j.virol.2015.06.006

Figure 3. Model of CVB dissemination in the host by shed EMVs.

Figure 3

High numbers of LC3II+ extracellular microvesicles (EMVs) containing infectious virus were recently observed following infection of progenitor cells in culture. Both the differentiation process and viral infection may enhance shedding of single membrane EMVs derived from the autophagy pathway. A) Virus-associated EMVs may expand the natural tropism of CV to target cells which fail to express canonical virus receptors. B) Neutralizing antibodies may be ineffective against infectious virus sequestered within the protected environment of the extracellular microvesicle. Also, virus-associated EMVs may increase the stability of infectious virus within the host during hematogenous spread. C) EMVs may assist in viral RNA dissemination during the persistent stage of infection whereby the presence of intact virions and/or structural viral proteins may be limited. D) EMVs may help virions travel and enter new target tissues and cross selectively permeable barriers.