Estimation of the Size of Genetic Bottlenecks in Cell-to-Cell Movement of
 Soil-
 Borne Wheat Mosaic Virus
 and the Possible Role of the Bottlenecks in Speeding Up Selection of Variations in
 trans
 -Acting Genes or Elements

Miyashita, Shuhei; Kishino, Hirohisa

doi:10.1128/jvi.01890-09

Cited by 90 publications

(113 citation statements)

References 36 publications

(28 reference statements)

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“…Each cell was infected by the viral population of the previous cell in the row. We are aware that this is probably an oversimplified model of plant cell connections, but we used it because it has been developed previously, applied, and discussed for the estimate of the MOI of another plant virus (30), allowing a direct comparison.…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, thus far, formally connecting these coinfection patterns to distinct MOIs is difficult due to the paucity of data. The MOI has been quantified in only a few multicellular host-virus models: an insect virus (27), an arbovirus in its mosquito vector (28), four plant viruses (each in a different host) (26,(29)(30)(31)(32), and HIV (33)(34)(35). In all cases the estimated values ranged from one to a few genome units per cell, suggesting that the MOI generally is low.…”

Section: Importancementioning

confidence: 99%

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The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus

Gutiérrez

Pirolles

Yvon

et al. 2015

J Virol

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The multiplicity of cellular infection (MOI) is the number of virus genomes of a given virus species that infect individual cells. This parameter chiefly impacts the severity of within-host population bottlenecks as well as the intensity of genetic exchange, competition, and complementation among viral genotypes. Only a few formal estimations of the MOI currently are available, and most theoretical reports have considered this parameter as constant within the infected host. Nevertheless, the colonization of a multicellular host is a complex process during which the MOI may dramatically change in different organs and at different stages of the infection. IMPORTANCEThe MOI is the size of the viral population colonizing cells and defines major phenomena in virus evolution, like the intensity of genetic exchange and the size of within-host population bottlenecks. However, few studies have quantified the MOI, and most consider this parameter as constant during infection. Our results reveal that the MOI can depend largely on the route of cell infection in a systemically infected leaf. The MOI is usually one genome per cell when cells are infected from virus particles moving long distances in the vasculature, whereas it is much higher during subsequent cell-to-cell movement in mesophyll. However, a fast-acting superinfection exclusion prevents cell coinfection by merging populations originating from different primary foci within a leaf. This complex colonization pattern results in a situation where within-cell interactions are occurring almost exclusively among kin and explains the common but uncharacterized phenomenon of genotype spatial segregation in infected plants.V iral populations can evolve rapidly, even during a single host infection, and the resulting changes in the population ultimately can affect the outcome of viral diseases. A clear example of this is the emergence of drug-resistant mutants of animal/human viruses, of resistance-breaking variants of plant viruses, or of recombinant genotypes with an enlarged host range. Therefore, it is not surprising that increasing efforts are being made to characterize parameters defining within-host evolution of viral populations.Since viruses are obligate intracellular parasites, a fundamental parameter determining their within-host population dynamics/ genetics is the multiplicity of cellular infection (MOI), defined as the number of genomes of a given virus species that infects a cell. The MOI influences two major processes in viral evolution, namely, the population bottlenecks and the interactions among genotypes. Within-host bottlenecks are linked to the number of infected cells during host colonization and to the MOI at which these cells are infected. The overall intensity of interactions among viral genomes, i.e., competition, genetic exchange, functional complementation, and collective action, depends to a large extent on the probability of encountering different genotypes within host cells, a probability that is directly linked to the MOI. Given the ...

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Section: Discussionmentioning

confidence: 99%

Section: Importancementioning

confidence: 99%

The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus

Gutiérrez

Pirolles

Yvon

et al. 2015

J Virol

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“…Studies of plant RNA viruses generally report small effective population sizes during transmission, whereas studies with one plant DNA virus reported a large population of virions during spread in single plant (21)(22)(23). The transmission of HIV between T cells involves transmission of a large number of virions across a virological synapse (2,24).…”

Section: Discussionmentioning

confidence: 99%

Alphaherpesvirus axon-to-cell spread involves limited virion transmission

Taylor

Kobiler

Enquist

2012

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

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The spread of viral infection within a host can be restricted by bottlenecks that limit the size and diversity of the viral population. An essential process for alphaherpesvirus infection is spread from axons of peripheral nervous system neurons to cells in peripheral epithelia (anterograde-directed spread, ADS). ADS is necessary for the formation of vesicular lesions characteristic of reactivated herpesvirus infections; however, the number of virions transmitted is unknown. We have developed two methods to quantitate ADS events using a compartmentalized neuronal culture system. The first method uses HSV-1 and pseudorabies virus recombinants that express one of three different fluorescent proteins. The fluorescence profiles of cells infected with the virus mixtures are used to quantify the number of expressed viral genomes. Strikingly, although epithelial or neuronal cells express 3-10 viral genomes after infection by free virions, epithelial cells infected by HSV-1 or pseudorabies virus following ADS express fewer than two viral genomes. The second method uses live-cell fluorescence microscopy to track individual capsids involved in ADS. We observed that most ADS events involve a single capsid infecting a target epithelial cell. Together, these complementary analyses reveal that ADS events are restricted to small numbers of viral particles, most often a single virion, resulting in a single viral genome initiating infection.cell-cell spread | live-cell imaging

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“…The multiplicity of infection (MOI), that is, the number of virus particles or genomes that infect a cell, has been estimated for some plant viruses either in local infections or along the systemic colonization of a host [66][67][68], giving roughly similar results, and showing that MOI may vary during systemic infection. Also, estimates of the size of genetic bottlenecks have been reported to be very low, associated to the systemic invasion of leaves [65], aphid transmission [58,69] and contact transmission [64] between hosts.…”

Section: Genetic Driftmentioning

confidence: 99%

Diversity of Plant Virus Populations: A Valuable Tool for Epidemiological Studies

Escriu¹

2017

Genetic Diversity

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Plant viruses, as any other living organisms, differ genetically from each other as a result of processes (such as mutation, recombination and other forms of genetic exchange) that generate genetic variation in each generation during their reproduction and processes (such as selection, migration and genetic drift) that modulate this variation, determine the distribution of the genetic variants within a population (i.e., the genetic structure of the population) and how it changes with time, in a dynamical phenomenon called evolution. For plant viruses, evolutionary forces that generate and modulate the genetic diversity of their populations are often associated to different phases in their biology and ecology, such as virus-host interactions and host to host transmission. Forces that shape the evolution of plant viruses are at the same time key factors affecting their pathogenic properties, including their ability to cause diseases (an aspect that is studied in the field of epidemiology). The present chapter aims to illustrate how measurement and analysis of genetic diversity and structure of plant virus populations are essential to the current knowledge on the evolutionary biology of plant viruses and how evolutionary factors have a relevant role in the dynamics of virus populations and therefore, in the epidemiology of plant virus diseases.

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Estimation of the Size of Genetic Bottlenecks in Cell-to-Cell Movement of Soil- Borne Wheat Mosaic Virus and the Possible Role of the Bottlenecks in Speeding Up Selection of Variations in trans -Acting Genes or Elements

Cited by 90 publications

References 36 publications

The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus

The Multiplicity of Cellular Infection Changes Depending on the Route of Cell Infection in a Plant Virus

Alphaherpesvirus axon-to-cell spread involves limited virion transmission

Diversity of Plant Virus Populations: A Valuable Tool for Epidemiological Studies

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