Evolution and Emergence of Plant Viruses

Elena, Santiago F.; Fraile, Aurora; García‐Arenal, Fernando

doi:10.1016/b978-0-12-800098-4.00003-9

Cited by 182 publications

(182 citation statements)

References 131 publications

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“…It is often considered that RNA viruses have a high potential to adapt to new hosts because their high census numbers and the high error rates of RNA-dependent RNA polymerases will translate into a strong potential to generate host range mutants (1,5,44). However, RNA viruses have small, information-compact genomes encoding few multifunctional proteins, which will favor pleiotropic effects of mutations (5,45).…”

Section: Discussionmentioning

confidence: 99%

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Mutations That Determine Resistance Breaking in a Plant RNA Virus Have Pleiotropic Effects on Its Fitness That Depend on the Host Environment and on the Type, Single or Mixed, of Infection

Moreno‐Pérez

García-Luque

Fraile

et al. 2016

J Virol

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Overcoming host resistance in gene-for-gene host-virus interactions is an important instance of host range expansion, which can be hindered by across-host fitness trade-offs. Trade-offs are generated by negative effects of host range mutations on the virus fitness in the original host, i.e., by antagonistic pleiotropy. It has been reported that different mutations in Pepper mild mottle virus (PMMoV) coat protein result in overcoming L-gene resistance in pepper. To analyze if resistance-breaking mutations in PMMoV result in antagonistic pleiotropy, all reported mutations determining the overcoming of L 3 and L 4 alleles were introduced in biologically active cDNA clones. Then, the parental and mutant virus genotypes were assayed in susceptible pepper genotypes with an L ؉ , L 1 , or L 2 allele, in single and in mixed infections. Resistance-breaking mutations had pleiotropic effects on the virus fitness that, according to the specific mutation, the host genotype, and the type of infection, single or mixed with other virus genotypes, were antagonistic or positive. Thus, resistance-breaking mutations can generate fitness trade-offs both across hosts and across types of infection, and the frequency of host range mutants will depend on the genetic structure of the host population and on the frequency of mixed infections by different virus genotypes. Also, resistance-breaking mutations variously affected virulence, which may further influence the evolution of host range expansion. Changes in virus host range affect virus ecology and epidemiology, condition virus emergence, and can compromise the success of strategies for the control of viral diseases (1-4). The acquisition of new hosts, that is, host range expansion, would provide a virus with more opportunities for transmission and survival. However, differential host-associated selection may result in across-host fitness trade-offs so that increasing the virus fitness in a new host will decrease its fitness in the original one, which will hinder host range expansion (4-6). The simplest mechanism generating across-hosts fitness trade-offs is antagonistic pleiotropy, in which mutations that increase fitness in one host are deleterious in another one (7). Evidence indicates that antagonistic pleiotropy is common in RNA viruses as a result of their small genomes, which are compacted with genetic information and encode few, multifunctional proteins (5,8).Host range evolution is particularly relevant for the sustainable use of genetic resistance to control viral diseases of crops. Disease control based on resistant cultivars is target specific and highly efficient but is not durable due to the appearance of new virus genotypes able to infect otherwise resistant host genotypes. The increase in frequency of resistance-breaking virus genotypes eventually renders resistance inefficient (9-11). Plant-virus interactions can often be explained by the gene-for-gene (GFG) model, under which direct or indirect recognition of viral proteins by those encoded by plant resistan...

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Section: Discussionmentioning

confidence: 99%

“…hanges in virus host range affect virus ecology and epidemiology, condition virus emergence, and can compromise the success of strategies for the control of viral diseases (1)(2)(3)(4). The acquisition of new hosts, that is, host range expansion, would provide a virus with more opportunities for transmission and survival.…”

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confidence: 99%

Mutations That Determine Resistance Breaking in a Plant RNA Virus Have Pleiotropic Effects on Its Fitness That Depend on the Host Environment and on the Type, Single or Mixed, of Infection

Moreno‐Pérez

García-Luque

Fraile

et al. 2016

J Virol

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“…7). Many studies have suggested that trade-offs are observed for plant virus infection across hosts, and antagonistic pleiotropy (when mutations beneficial for infection of one host are deleterious for infection of another one) explains such trade-offs well (56,57). For example, tobacco etch virus (TEV) infects several solanaceous plants, such as Nicotiana tabacum, in nature, and some nonsolanaceous plants (e.g., Helianthus annuus and Spinacia oleracea) are also susceptible under experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

Atsumi

Suzuki

Miyashita

et al. 2016

J Virol

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IMPORTANCEControl of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred by cyv1, mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in a cyv1-carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance (cyv1) and host viability; the latter is presumably regulated by the dominant Cyn1 gene, which may impose evolutionary constraints upon P3N-PIPO for overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.H ost plants protect themselves from virus infection by activating defense systems mediated by immune receptors (e.g., nucleotide-binding-site-leucine-rich-repeat [NB-LRR] proteins) (1). Plants have many NB-LRR immune receptors, each of which recognizes specific viral proteins. The activated immune response is referred to as a hypersensitive response (HR) and is often accompanied by cell death. When an HR is induced, the virus is localized in and around the infection locus. NB-LRR immune receptors are encoded by resistance genes that are genetically dominant.Another important defense against plant virus infection is genetically recessive resistance (2). The viral life cycle totally relies on host cells, and viruses require host factors in order to multiply within cells and move to neighboring cells. Therefore, the lack of a specific host-coopted factor required for the viral life cycle leads to host resistance against the virus, which would be recessively inherited. Many natural recessive resistance genes against viruses have been identified in diverse crops (2). Extensive studies have been carried out on viruses belonging to the Potyvirus genus, the major genus of the Potyviridae family, which is one of the two largest plant virus genera and is found in most climatic regions worldwide (3). These viruses infect a broad range of host plants, including both monocots and dicots. They cause considerable crop damage, resulting in severe economic losses. Most of the recessive

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“…Here, it is important to stress that the symplast, where plant viruses must replicate and evolve, is a high structured environment where virus populations adopt a metapopulation structure, a set of subpopulations, each one occupying different tissues and organs. This metapopulation structure is probably generated by the effect of genetic bottlenecks and might affect the efficiency of natural selection [80]. In the third phase, an efficient epidemiology should optimize between-host transmission in the new host and environment, which implies new adaptation to vectors in the case of vectored viruses.…”

Section: Dynamics Of Genetic Diversity and Structure Of Plant Virus Pmentioning

confidence: 99%

“…Ecological and epidemiological factors of plant virus emergence often have their origin at the interface between managed and natural ecosystems and are mostly related to a rapid expansion of human activity, including the worldwide distribution of crop species far from their geographic origins, the intensiveness of agricultural practices and the international trade facilitating the spread of damaging viral species, all of them under the effect of global climate change [79]. Factors favoring emergence derive from complex interactions among host plants, viruses and their vectors (for vector-borne viruses) and have been analyzed in the context of evolutionary ecology, genetics and epidemiology [80]. In summary, they result in changes in the ecology and genetic composition of host plant, virus and vector populations during three different temporal phases that describe the process of emergence.…”

Section: Dynamics Of Genetic Diversity and Structure Of Plant Virus Pmentioning

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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Evolution and Emergence of Plant Viruses

Cited by 182 publications

References 131 publications

Mutations That Determine Resistance Breaking in a Plant RNA Virus Have Pleiotropic Effects on Its Fitness That Depend on the Host Environment and on the Type, Single or Mixed, of Infection

Mutations That Determine Resistance Breaking in a Plant RNA Virus Have Pleiotropic Effects on Its Fitness That Depend on the Host Environment and on the Type, Single or Mixed, of Infection

P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

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

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