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2000
Volume 21, Issue 6
  • ISSN: 1389-2029
  • E-ISSN: 1875-5488

Abstract

Viruses are obligate parasites that exist in an inactive state until they enter the host body. Upon entry, viruses become active and start replicating by using the host cell machinery. All plant viruses can augment their transmission, thus powering their detrimental effects on the host plant. To diminish infection and diseases caused by viruses, the plant has a defence mechanism known as pathogenesis- related biochemicals, which are metabolites and proteins. Proteins that ultimately prevent pathogenic diseases are called R proteins. Several plant R genes (that confirm resistance) and avirulence protein (Avr) (pathogen Avr gene-encoded proteins [effector/elicitor proteins involved in pathogenicity]) molecules have been identified. The recognition of such a factor results in the plant defence mechanism. During plant viral infection, the replication and expression of a viral molecule lead to a series of a hypersensitive response (HR) and affect the host plant’s immunity (pathogen-associated molecular pattern–triggered immunity and effector-triggered immunity). Avr protein renders the host RNA silencing mechanism and its innate immunity, chiefly known as silencing suppressors towards the plant defensive machinery. This is a strong reply to the plant defensive machinery by harmful plant viruses. In this review, we describe the plant pathogen resistance protein and how these proteins regulate host immunity during plant–virus interactions. Furthermore, we have discussed regarding ribosome- inactivating proteins, ubiquitin proteasome system, translation repression (nuclear shuttle protein interacting kinase 1), DNA methylation, dominant resistance genes, and autophagy-mediated protein degradation, which are crucial in antiviral defences.

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/content/journals/cg/10.2174/1389202921999200712135131
2020-09-01
2025-09-03
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/content/journals/cg/10.2174/1389202921999200712135131
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