Virus and Host Plant Interactions

Abstract

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.

Turnip mosaic virus P1 suppresses JA biosynthesis by degrading cpSRP54 that delivers AOCs onto the thylakoid membrane to facilitate viral infection

“…The hypothesis that cpSRP54 acts upstream of JA biosynthesis and in the context of a relatively conserved antiviral defense role of JA, is supported by our findings that PMMoV and PVX infection could also downregulate the protein level of cpSRP54, which implies that cpSRP54 is a common target for various viruses to combat JA-mediated defense. It is notable that transcripts of cpSRP54 were also downregulated in TuMV-infected plants, which indicates a possible mechanism by which TuMV regulates JA synthesis at the transcriptional level (S1C Fig) . In addition to manipulating the JA pathway, plant viruses strike back on every aspect of plant defense, including RNA silencing, the ubiquitin proteosome system or autophagy, translation repression, other defense hormone and hormone regulatory pathways, and plant innate immunity, to win the arms race [54,55]. Some conserved core elements, such as the JAZ-MYC hub in JA signaling, rice auxin response factor 17 (OsARF17) in auxin signaling, and Argonaute 1 (AGO1) in RNA silencing defense pathway, have been shown to be convergently targeted by various viruses.…”