Plant–Virus Interactions: Defence and Counter‐Defence

Abstract

Viruses replicate in intimate association with their host cells. This has influenced the means by which plants defend themselves against viruses and the strategies adopted by viruses to exploit host plants. In this chapter, we examine howRgene‐mediated resistance against specific avirulent viral pathogens differs in important respects from resistance against non‐viral pathogens (bacteria, fungi, oomycetes, etc.) while utilising many of the same signal transduction pathways. We also explore mechanisms of recessive gene‐mediated resistance to viruses and genetically determined resistance to viral movement. Finally, we describe the emergence of host RNA silencing pathways as key determinants of the outcome of most plant–virus interactions. These pathways can act as important effectors of basal and induced resistance to viruses. Additionally, RNA silencing pathways can act as targets for viral suppressor proteins. Disruption of silencing pathways is the predominant means by which viruses induce disease symptoms in susceptible plant hosts.

R-BPMV-Mediated Resistance to Bean pod mottle virus in Phaseolus vulgaris L. Is Heat-Stable but Elevated Temperatures Boost Viral Infection in Susceptible Genotypes

“…Interestingly, at 7 dpi, we observed larger HR lesions at 25 and 30 • C compared to 20 • C, and this observation was correlated with (i) more expanded multiplication areas of BPMV visualized as green fluorescence areas in BPMV-GFP infected leaves at 4 dpi (Figure 2) and (ii) a rising virus titer in the inoculated leaves at 7 dpi (Figure 3B,C). Consequently, we propose that the higher levels of BPMV accumulation and cell-to-cell spreading in the primary sites of infection could be attributed to a delayed defense response when temperature increases from 20 to 30 • C. As biotrophic pathogens, viruses mainly induce defense responses regulated by salicylic acid (SA) signaling [74], and SA was shown to be a key component that orchestrates the events restricting viral spread in HR [75,76]. Moreover, HR-mediated resistance against Turnip crinkle virus (TCV) was impaired in Arabidopsis eds5 and sid2 SA-deficient mutants without affecting HR cell death [77].…”

“…Consequently, we propose that the higher levels of BPMV accumulation and cell-to-cell spreading in the primary sites of infection could be attributed to a delayed defense response when temperature increases from 20 to 30 °C. As biotrophic pathogens, viruses mainly induce defense responses regulated by salicylic acid (SA) signaling [ 74 ], and SA was shown to be a key component that orchestrates the events restricting viral spread in HR [ 75 , 76 ]. Moreover, HR-mediated resistance against Turnip crinkle virus (TCV) was impaired in Arabidopsis eds5 and sid2 SA-deficient mutants without affecting HR cell death [ 77 ].…”

Engineering Resistance Against Viruses in Field Crops Using CRISPRCas9

“…The key components of the RNA silencing pathways are the existence of multiple copies of AGO (Argonaute), DRB (double-stranded RNA binding), RNA dependent RNA polymerase (RDR) and DCL (Dicer-like) genes, which play an important protective role against invading viral pathogens [ 108 , 109 ]. However, RNAi-mediated resistance is regularly hindered by several co-evolving viral suppressors (VSRs), which could enhance the viral pathogenicity within susceptible hosts [ 110 ].…”

Epigenetic Changes in Host Ribosomal DNA Promoter Induced by an Asymptomatic Plant Virus Infection

“…Viruses, as obligate intracellular parasites, establish complex relationships with their hosts [1,2]. This type of relationship imposes numerous challenges on both the infecting virus and the host partner [3,4].…”