Bunyavirus superinfection and segment reassortment in transovarially infected mosquitoes

Borucki, Monica K.; Chandler, Laura J.; Parker, Beulah M.; Blair, Carol D.; Beaty, Barry J.

doi:10.1099/0022-1317-80-12-3173

Cited by 55 publications

(36 citation statements)

References 22 publications

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“…Genome recruitment is expected to be similar in all phleboviruses, thus the conserved hydrophobic pocket of N is a candidate G N binding site. This hypothesis is consistent with the ability of bunyaviruses, both in nature and in vitro, to undergo reassortment in which progeny have genomic segments that derive from more than one parental virus (32)(33)(34). Reassortment requires promiscuity in the interaction of N with genomic RNAs from heterologous viruses and in protein-protein interactions necessary for assembling virions.…”

Section: Discussionsupporting

confidence: 79%

Structure of the Rift Valley fever virus nucleocapsid protein reveals another architecture for RNA encapsidation

Raymond¹,

Piper²,

Gerrard

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

115

144

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Rift Valley fever virus (RVFV) is a negative-sense RNA virus (genus Phlebovirus, family Bunyaviridae) that infects livestock and humans and is endemic to sub-Saharan Africa. Like all negative-sense viruses, the segmented RNA genome of RVFV is encapsidated by a nucleocapsid protein (N). The 1.93-Å crystal structure of RVFV N and electron micrographs of ribonucleoprotein (RNP) reveal an encapsidated genome of substantially different organization than in other negative-sense RNA virus families. The RNP polymer, viewed in electron micrographs of both virus RNP and RNP reconstituted from purified N with a defined RNA, has an extended structure without helical symmetry. N-RNA species of ∼100-kDa apparent molecular weight and heterogeneous composition were obtained by exhaustive ribonuclease treatment of virus RNP, by recombinant expression of N, and by reconstitution from purified N and an RNA oligomer. RNA-free N, obtained by denaturation and refolding, has a novel all-helical fold that is compact and well ordered at both the N and C termini. Unlike N of other negative-sense RNA viruses, RVFV N has no positively charged surface cleft for RNA binding and no protruding termini or loops to stabilize a defined N-RNA oligomer or RNP helix. A potential protein interaction site was identified in a conserved hydrophobic pocket. The nonhelical appearance of phlebovirus RNP, the heterogeneous ∼100-kDa N-RNA multimer, and the N fold differ substantially from the RNP and N of other negative-sense RNA virus families and provide valuable insights into the structure of the encapsidated phlebovirus genome.ribonucleoprotein | viral protein | segmented genome | negative-sense RNA virus

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Section: Discussionsupporting

confidence: 79%

Structure of the Rift Valley fever virus nucleocapsid protein reveals another architecture for RNA encapsidation

Raymond¹,

Piper²,

Gerrard

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

115

144

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“…Although reassortment of the tripartite orthobunyaviral genome, comprising segments designated small (S), medium (M), and large (L), has been shown experimentally to occur easily between genetically related viruses (2,3,10,19), examples of natural reassortment have not frequently been described for Bunyamwera or California serogroup viruses (16). Recently, Ngari virus (NRIV) was recognized as a natural reassortant virus associated with a hemorrhagic fever outbreak in Kenya and Somalia (4,11).…”

mentioning

confidence: 99%

Batai and Ngari Viruses: M Segment Reassortment and Association with Severe Febrile Disease Outbreaks in East Africa

Briese

Bird

Kapoor

et al. 2006

J Virol

140

144

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“…It has been suggested that genome segmentation can help counteract the effects of deleterious mutations by allowing the virus to undergo reassortment [145,146], which may be caused by the selection of shorter RNA molecules whose replication can be completed within a shorter time frame [147,148]. Reassortment events have been described within the family Bunyaviridae and occur mainly in dually infected mosquitoes when the two viruses are ingested within 48 h [149]. In bacteriophages, the viral genome can be partially dehydrated inside the capsid if its size exceeds a particular threshold.…”

Section: • • Bunyavirusesmentioning

confidence: 99%

Arboviruses: Variations on an Ancient Theme

et al. 2014

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Arboviruses utilize different strategies to complete their transmission cycle between vertebrate and invertebrate hosts. Most possess an RNA genome coupled with an RNA polymerase lacking proofreading activity and generate large populations of genetically distinct variants, permitting rapid adaptation to environmental changes. With mutation rates of between 10 -6 and 10 -4 substitutions per nucleotide, arboviral genomes rapidly acquire mutations that can lead to viral emergence. Arboviruses can be described in seven families, four of which have medical importance: Togaviridae, Flaviviridae, Bunyaviridae and Reoviridae. The Togaviridae and Flaviviridae both have ssRNA genomes, while the Bunyaviridae and Reoviridae possess segmented RNA genomes. Recent epidemics caused by these arboviruses have been associated with specific mutations leading to enhanced host ranges, vector shifts and virulence. KEYWORDS Arboviruses: the role of RNA genomes in viral adaptation & emergenceThe recent emergence of many arboviruses (i.e., West Nile virus [WNV] in North America [1] and Chikungunya virus [CHIKV] in the Indian Ocean islands [2]) serves as a reminder that these viruses are capable of rapidly adapting to changes in their environment. Such viral epidemics can often be associated with the accumulation of one or more specific mutations in the viral genome and highlight a hallmark feature of arboviruses [3][4][5][6]. Indeed, arboviruses, and many other RNA viruses, employ a unique feature of their RNA-dependent RNA polymerases in order to achieve this rapid adaptation: inaccuracy due to a lack of proofreading activity [7][8][9]. This inaccuracy is the result of evolutionary pressure related to the fidelity of the polymerase. Mutations that decrease the fidelity of viral polymerases, have been shown to cause the accumulation of attenuating and lethal mutations [10], while mutations that enhance the fidelity of the polymerase are also associated with attenuation due to a reduction in the number of viral quasispecies, leaving the virus unable to cope with sudden environmental changes within the host [11]. These studies and others have shown that RNA virus replication balances on a 'knife's edge', with slight changes in their fidelity leading to population collapse [12]. Arboviruses are further constrained by the need to replicate in both a vector and a host species. These two very dissimilar organisms each place unique selective pressures on the arboviral genome, such that mutations that adapt the virus to favor one host are often deleterious in the other host [13][14][15]. Despite this evolutionary pressure, many arboviruses have expanded both their geographical distribution and host range through the generation and accumulation of beneficial mutations [16,17].The major source of these mutations comes from errors that occur during genome replication. Mutation rates during viral RNA replication are in the range of 10 -6 -10 -4 substitutions per For reprint orders, please contact: reprints@futuremedicine.com

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Bunyavirus superinfection and segment reassortment in transovarially infected mosquitoes

Cited by 55 publications

References 22 publications

Structure of the Rift Valley fever virus nucleocapsid protein reveals another architecture for RNA encapsidation

Structure of the Rift Valley fever virus nucleocapsid protein reveals another architecture for RNA encapsidation

Batai and Ngari Viruses: M Segment Reassortment and Association with Severe Febrile Disease Outbreaks in East Africa

Arboviruses: Variations on an Ancient Theme

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