Virus and Host Plant Interactions


Plant viruses infect almost all crops and cause serious diseases worldwide. Currently, viral pathogens account for the largest proportion of newly emerging plant diseases and as such, are considered a major constraint to agriculture, threatening global food security. All plant viruses have relatively small genomes with limited coding capacity. They must co‐opt cellular pathways and recruit host proteins and metabolites to complete their infection cycle. To combat virus infection, plants have evolved sophisticated defence mechanisms. In order to establish infection, viruses have also evolved virulence strategies to suppress host defence. A successful infection by a plant virus requires compatible molecular interplays between the host plant and the invading virus. A better understanding of the complex virus–plant interactions will assist in the development of novel antiviral strategies.

Key Concepts

  • Plant viruses have small genomes that encode a few proteins and thus depend on host factors to establish their infection.
  • There exist multifaceted defence and counterdefence strategies in the coevolutionary arms race between plants and viruses.
  • A successful viral infection may induce disease symptoms or remain asymptomatic.
  • Host factors are implicated in all steps of the viral infection process, and silencing or mutation of host factor gene(s) leads to recessive genetic resistance to viruses.
  • The majority host factors are also essential for plant viability and some of them may be manipulated to develop genetic resistance through precise mutation to retain their canonical cellular functions but lose the ability to support viral infection.

Keywords: viral pathogenesis; RNA silencing; viral suppressor of RNA silencing; plant immunity; viral replication complex; chloroplasts; plant hormones; viral intercellular movement; viral long‐distance transport

Figure 1. Suppression of RNA (ribonucleic acid) silencing by VSRs (viral suppressors of RNA silencing). (a) Antiviral RNA silencing pathways and suppression mechanisms of VSRs. Upon viral infection, viral dsRNA derived from viral replication, de novo synthesis by cellular RDR6 and intramolecular pairing are recognised by Dicer‐like enzymes to generate viral small interfering ribonucleic acids (vsiRNAs). Aberrant (Ab) RNAs from viral replication or DCL processing are used as template by RDR6 to generate dsRNAs, which are subjected to DCL processing. The resulting 20‐ to 24‐nt RNA duplexes are incorporated into the RNA‐induced silencing complex (RISC). The loaded vsiRNAs guide the RISC to recognise the viral genome for silencing or translational repression. VSRs encoded by different viruses may suppress antiviral RNA at different stages of the silencing pathways. (b) A soybean plant infected by soybean mosaic virus (SMV) showing strong leaf symptoms. (c) Soybean seeds harvested from SMV‐infected plants. The mottling phenotype was caused by the suppression of natural RNA silencing‐mediated degradation of the CHS gene transcripts by the SMV VSR (Senda et al., ).
Figure 2. Defence and counterdefence in the coevolutionary arms race between potyviruses and plant hosts. Potyviruses are the largest group of known plant viruses. The potyviral genome encodes two polyproteins that are processed into 11 viral proteins (VRs) including coat protein (CP), nuclear inclusion b (NIb), which is the only viral RNA‐dependent RNA polymerase (RdRp), and two VSRs HC‐Pro and VPg. Potyviral dsRNAs trigger antiviral RNA silencing and also induce PAMP‐triggered immunity (PTI) as a pathogen‐associated molecular pattern (PAMP). Potyviral CP suppresses PTI as a virus‐encoded innate immunity suppressor. VSRs counteract RNA silencing and also regulate effector‐triggered immunity (ETI) by suppression of cellular DCL4‐dependent small interference RNAs that modulate the expression of resistance (R) genes coding for nucleotide‐binding site leucine‐rich repeats (NB‐LRR) receptors. PTI can be activated by PTI acceptors BAK1 and SERK1. In some cases, the resistance signalling leads to the hypersensitive response (HR), necrosis and systemic acquired resistance (SAR), which are accompanied with enhanced levels of salicylic acid (SA), jasmonic acid (JA), ethylene (ET), nitric oxide (NO) and hydrogen peroxide (H2O2). In this process, many defence genes are upregulated. One master regulator is nonexpressor of pathogenesis‐related genes‐1 (NPR1). Small ubiquitin‐like modifier 3 (SUMO3) is an activator of NPR1. Potyviral NIb represses NPR1 possibly through depletion of SUMO3 to promote viral infection. Modified with permission from Cheng and Wang 2017 © Taylor and Francis.
Figure 3. Chloroplast and viral pathogenesis. (a) An electron micrograph showing part of a chloroplast from a Chinese cabbage leaf cell infected by TYMV. The arrow points to a vesicle in which an open channel is apparently connecting the interior to the cytoplasm. Bar = 100 nm. Adapted with permission from Prod'homme et al. 2001 © Academic Press. (b) Confocal micrographs showing colocalisation of virus replication vesicles with 6K2 bodies associated with aggregated chloroplasts in protoplasts isolated from Nicotiana benthamiana leaf tissues infected by a recombinant TuMV containing additional 6K2 tagged by GFP. DsRNA signals derived from staining with monoclonal antibody J2; DIC, differential interference contrast; Chl, chlorophyll autofluorescence (in blue). Bar = 8 µm. Adapted from with permission Wei et al. 2010a © American Society for Microbiology. (c) The impact of viral infection on chloroplast. In virus‐infected cells, some viral proteins (VPs) physically interact with the nucleus‐encoded chloroplast proteins (ncChlPs), while some other are involved in regulation of the expression of ncChlps. In general, viral infection induces the expression of defence genes and suppresses the expression of chloroplast‐ and photosynthesis‐related genes. Adapted from Li et al. 2016, with permission from Elsevier.
Figure 4. Cell‐to‐cell movement of potyviruses. (a,b) Electron micrographs showing the conical structures of CI at PD that enters a neighbouring cell in a linear form (arrows) traversing the cell wall (CW) in leaf tissues infected by sorghum mosaic virus. 100 nm. (c) Model for potyviral intercellular transport. The PD‐located P3N‐PIPO directs the CI to form conical structures at the PD and possibly increase the aperture of PD. The movement complex that is comprised of virion, CI, HC‐Pro and host factors targets the CI‐modified PD. The virion, guided by the CI structure, penetrates through the PD and enters the neighbouring cell. PSI, photosystem I; PSII, photosystem II. Reproduced with permission from Wei et al. 2010b © PLOS.


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Further Reading

Brunkard JQ and Zambrysi PC (2017) Plasmodesmata enable multicellularity: new insights into their evolution, biogenesis, and functions in development and immunity. Current Opinion in Plant Biology 35: 76–83.

Caranta C, Aranda MA, Tepfer M and López‐Moya JJ (2011) Recent Advances in Plant Virology. Norfolk: Caister Academic Press.

Hull R (2014) Plant Virology, 5th edn. London: Academic Press.

Wang A (2010) Principles and Practice of Advanced Technology in Plant Virology. Kerala: Research Signpost.

Wang A and Zhou X (2016) Current Research Topics in Plant Virology. Switzerland: Springer.

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Wang, Aiming(Feb 2018) Virus and Host Plant Interactions. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000758.pub3]