Recovery from virus infection: plant's armory in action

Main conclusionThis review focuses on different factors involved in promoting symptom recovery in plants post-virus infection such as epigenetics, transcriptional reprogramming, phytohormones with an emphasis on RNA silencing as well as role of abiotic factors such as temperature on symptom recovery.Plants utilize several different strategies to defend themselves in the battle against invading viruses. Most of the viral proteins interact with plant proteins and interfere with molecular dynamics in a cell which eventually results in symptom development. This initial symptom development is countered by the plant utilizing various factors including the plant's adaptive immunity to develop a virus tolerant state. Infected plants can specifically target and impede the transcription of viral genes as well as degrade the viral transcripts to restrict their proliferation by the production of small-interfering RNA (siRNA) generated from the viral nucleic acid, known as virus-derived siRNA (vsiRNA). To further escalate the degradation of viral nucleic acid, secondary siRNAs are generated. The production of virus-activated siRNA (vasiRNA) from the host genome causes differential regulation of the host transcriptome which plays a major role in establishing a virus tolerant state within the infected plant. The systemic action of vsiRNAs, vasiRNA, and secondary siRNAs with the help of defense hormones like salicylic acid can curb viral proliferation, and thus the newly emerged leaves develop fewer symptoms, maintaining a state of tolerance.

Automated summary

This review explores various factors involved in promoting symptom recovery in plants post-virus infection, including epigenetics, transcriptional reprogramming, phytohormones, and RNA silencing. It also discusses the influence of abiotic factors such as temperature. Plants utilize different strategies, including adaptive immunity and production of small-interfering RNA, to defend against virus infection and establish a virus tolerant state by targeting viral genes and degrading viral transcripts. This leads to a reduction in symptom development and the establishment of tolerance.