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dc.contributor.authorCifuentes-Muñoz N.
dc.contributor.authorEllis Dutch R.
dc.date.accessioned2020-09-02T22:14:52Z
dc.date.available2020-09-02T22:14:52Z
dc.date.issued2019
dc.identifier10.1016/j.virusres.2019.03.002
dc.identifier.citation265, , 68-73
dc.identifier.issn01681702
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4023
dc.descriptionPneumoviruses represent a major public health burden across the world. Respiratory syncytial virus (RSV) and human metapneumovirus (HMPV), two of the most recognizable pediatric infectious agents, belong to this family. These viruses are enveloped with a non-segmented negative-sense RNA genome, and their replication occurs in specialized cytosolic organelles named inclusion bodies (IB). The critical role of IBs in replication of pneumoviruses has begun to be elucidated, and our current understanding suggests they are highly dynamic structures. From IBs, newly synthesized nucleocapsids are transported to assembly sites, potentially via the actin cytoskeleton, to be incorporated into nascent virions. Released virions, which generally contain one genome, can then diffuse in the extracellular environment to target new cells and reinitiate the process of infection. This is a challenging business for virions, which must face several risks including the extracellular immune responses. In addition, several recent studies suggest that successful infection may be achieved more rapidly by multiple, rather than single, genomic copies being deposited into a target cell. Interestingly, recent data indicate that pneumoviruses have several mechanisms that permit their transmission en bloc, i.e. transmission of multiple genomes at the same time. These mechanisms include the well-studied syncytia formation as well as the newly described formation of long actin-based intercellular extensions. These not only permit en bloc viral transmission, but also bypass assembly of complete virions. In this review we describe several aspects of en bloc viral transmission and how these mechanisms are reshaping our understanding of pneumovirus replication, assembly and spread. © 2019 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectEn bloc
dc.subjectInclusion bodies
dc.subjectNucleocapsids
dc.subjectPneumoviruses
dc.subjectSpread
dc.subjectcell fusion
dc.subjectcell inclusion
dc.subjectgenome analysis
dc.subjecthuman
dc.subjectimmune response
dc.subjectintercellular space
dc.subjectnonhuman
dc.subjectPneumovirus
dc.subjectpolyploidy
dc.subjectpriority journal
dc.subjectReview
dc.subjectvirion
dc.subjectvirus assembly
dc.subjectvirus genome
dc.subjectvirus nucleocapsid
dc.subjectvirus replication
dc.subjectvirus transmission
dc.subjectanimal
dc.subjectcell line
dc.subjectgenetics
dc.subjectMetapneumovirus
dc.subjectmouse
dc.subjectparamyxovirus infection
dc.subjectphysiology
dc.subjectPneumovirus
dc.subjecttransmission
dc.subjectvirus RNA
dc.subjectAnimals
dc.subjectCell Line
dc.subjectHumans
dc.subjectMetapneumovirus
dc.subjectMice
dc.subjectParamyxoviridae Infections
dc.subjectPneumovirus
dc.subjectRNA, Viral
dc.subjectVirion
dc.subjectVirus Assembly
dc.subjectVirus Replication
dc.titleTo assemble or not to assemble: The changing rules of pneumovirus transmission
dc.typeReview


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