▪ Abstract Populations of plant viruses, like all other living beings, are genetically heterogeneous, a property long recognized in plant virology. Only recently have the processes resulting in genetic variation and diversity in virus populations and genetic structure been analyzed quantitatively. The subject of this review is the analysis of genetic variation, its quantification in plant virus populations, and what factors and processes determine the genetic structure of these populations and its temporal change. The high potential for genetic variation in plant viruses, through either mutation or genetic exchange by recombination or reassortment of genomic segments, need not necessarily result in high diversity of virus populations. Selection by factors such as the interaction of the virus with host plants and vectors and random genetic drift may in fact reduce genetic diversity in populations. There is evidence that negative selection results in virus-encoded proteins being not more variable than those of their hosts and vectors. Evidence suggests that small population diversity, and genetic stability, is the rule. Populations of plant viruses often consist of a few genetic variants and many infrequent variants. Their distribution may provide evidence of a population that is undifferentiated, differentiated by factors such as location, host plant, or time, or that fluctuates randomly in composition, depending on the virus.

Viruses are common agents of plant infectious diseases. During last decades, worldwide agriculture production has been compromised by a series of epidemics caused by new viruses that spilled over from reservoir species or by new variants of classic viruses that show new pathogenic and epidemiological properties. Virus emergence has been generally associated with ecological change or with intensive agronomical practices. However, the complete picture is much more complex since the viral populations constantly evolve and adapt to their new hosts and vectors. This chapter puts emergence of plant viruses into the framework of evolutionary ecology, genetics, and epidemiology. We will stress that viral emergence begins with the stochastic transmission of preexisting genetic variants from the reservoir to the new host, whose fate depends on their fitness on each hosts, followed by adaptation to new hosts or vectors, and finalizes with an efficient epidemiological spread.

Genetic resistance often fails because a resistance-breaking (RB) pathogen genotype increases in frequency. On the basis of an analysis of cellular plant pathogens, it was recently proposed that the evolutionary potential of a pathogen is a major determinant of the durability of resistance. We test this hypothesis for plant viruses, which differ substantially from cellular pathogens in the nature, size, and expression of their genomes. Our analysis was based on 29 plant virus species that provide a good representation of the genetic and biological diversity of plant viruses. These 29 viruses were involved in 35 pathosystems, and 50 resistance factors deployed against them were analyzed. Resistance was found to be durable more often than not, in contrast with resistance to cellular plant pathogens. In a third of the analyzed pathosystems RB strains have not been reported, and in another third RB strains have been reported but have not become prevalent in the virus population. The evolutionary potential of the viruses in the 35 pathosystems was evaluated with a compound risk index based on three evolutionary factors: the population of the pathogen, the degree of recombination, and the amount of gene and genotype flow. Our analysis indicates that evolutionary potential may be an important determinant of the durability of resistance against plant viruses.