Journal
ANNALS OF BOTANY
Volume 119, Issue 5, Pages 711-723Publisher
OXFORD UNIV PRESS
DOI: 10.1093/aob/mcw200
Keywords
Antiviral immunity; antiviral immune receptors; PAMP-triggered immunity; effector-triggered immunity; NSP-interacting kinase; NIK-mediated translation suppression; antiviral RNA silencing; hormone-mediated defence; proteasome degradation; NBS-LRR resistance protein; receptor-like kinase; LRR-RLK
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Funding
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [573600/2008-2, 447578/2014-6]
- Fundacao de Amparoa Pesquisa do Estado de Minas Gerais [CBB-APQ-03175-13, CBB-APQ-01491-14]
- CAPES graduate fellowship
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Background Among the environmental limitations that affect plant growth, viruses cause major crop losses worldwide and represent serious threats to food security. Significant advances in the field of plant-virus interactions have led to an expansion of potential strategies for genetically engineered resistance in crops during recent years. Nevertheless, the evolution of viral virulence represents a constant challenge in agriculture that has led to a continuing interest in the molecular mechanisms of plant-virus interactions that affect disease or resistance. Scope and Conclusion This review summarizes the molecular mechanisms of the antiviral immune system in plants and the latest breakthroughs reported in plant defence against viruses. Particular attention is given to the immune receptors and transduction pathways in antiviral innate immunity. Plants counteract viral infection with a sophisticated innate immune system that resembles the non-viral pathogenic system, which is broadly divided into pathogen-associated molecular pattern (PAMP)-triggered immunity and effector-triggered immunity. An additional recently uncovered virus-specific defence mechanism relies on host translation suppression mediated by a transmembrane immune receptor. In all cases, the recognition of the virus by the plant during infection is central for the activation of these innate defences, and, conversely, the detection of host plants enables the virus to activate virulence strategies. Plants also circumvent viral infection through RNA interference mechanisms by utilizing small RNAs, which are often suppressed by co-evolving virus suppressors. Additionally, plants defend themselves against viruses through hormone-mediated defences and activation of the ubiquitin-26S proteasome system (UPS), which alternatively impairs and facilitates viral infection. Therefore, plant defence and virulence strategies co-evolve and co-exist; hence, disease development is largely dependent on the extent and rate at which these opposing signals emerge in host and non-host interactions. A deeper understanding of plant antiviral immunity may facilitate innovative biotechnological, genetic and breeding approaches for crop protection and improvement.
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