Virus variation in relation to resistance-breaking in plants

Abstract

In plant viruses, genomic variation caused by mutation is enhanced by recombination, pseudo-recombination and acquisition of extra genomic components. Genomic RNA typically has a high mutation rate, and individual virus isolates consist of swarms of mutants, with the consensus sequence changing in response to selection pressure. Recombination is found among field isolates of some RNA viruses, especially tobraviruses. Among DNA viruses, field isolates of geminiviruses show unexpected nucleotide diversity and frequency of recombination, some of it interspecific. Recombination among whitefly-transmitted geminiviruses (begomoviruses) occurring in the same geographical region contributes to their evolutionary divergence, as a group. Several (perhaps potentially all) viral genes can encode an avirulence factor that elicits resistance controlled by a cognate dominant host gene: such factors include viral coat protein, RNA polymerase, movement protein and proteinase. Some resistance-breaking virus variants have merely a single nonsynonymous nucleotide replacement in their avirulence gene but, with more durable resistances, virulence necessitates two or even multiple replacements. The probability of a resistance-breaking variant appearing and spreading also depends on its biological fitness in the absence of the host resistance gene, and on the type of resistance and number of resistance genes to be overcome. Viruses can have particular difficulty in overcoming strong resistance controlled either by multiple recessive genes or by coat-protein transgenes. Resistance acting at the RNA level is exemplified by post-transcriptional gene silencing induced by transgenic viral sequences. This resistance may be broken by variants with >10% nucleotide non-identity distributed along the sequence. Our ability to identify, and potentially to create, durable virus resistance is increasing steadily.