Principles of Molecular Virology, Chapter 6 (Virus Infection), discusses virus infections of plants and animals, and examines the similarities and the differences between them.
I've been updating my lecture notes for students and writing self-assessment questions for the Principles of Molecular Virology website, and in the course of my research I came across the following useful articles about virus infection of plants - and how plants fight infection. All these are freely available via Open Access (search for the title of each paper on Google Scholar).
The first paper considers how virus infections of plants cause disease, although this is not an inevitable outcome of infection. As in animals, plant antiviral systems often contribute to symptoms of infection:
Pallas, V., & García, J. A. (2011) How do plant viruses induce disease? Interactions and interference with host components. Journal of General Virology, 92(12), 2691-2705 Abstract:
Plant viruses are biotrophic pathogens that need living tissue for their multiplication and thus, in the infection–defence equilibrium, they do not normally cause plant death. In some instances virus infection may have no apparent pathological effect or may even provide a selective advantage to the host, but in many cases it causes the symptomatic phenotypes of disease. These pathological phenotypes are the result of interference and/or competition for a substantial amount of host resources, which can disrupt host physiology to cause disease. This interference/competition affects a number of genes, which seems to be greater the more severe the symptoms that they cause. Induced or repressed genes belong to a broad range of cellular processes, such as hormonal regulation, cell cycle control and endogenous transport of macromolecules, among others. In addition, recent evidence indicates the existence of interplay between plant development and antiviral defence processes, and that interference among the common points of their signalling pathways can trigger pathological manifestations. This review provides an update on the latest advances in understanding how viruses affect substantial cellular processes, and how plant antiviral defences contribute to pathological phenotypes.
This paper discusses plant disease resistance (R) genes, the equivalent to the immune system in animals:
Gururani, M. A., Venkatesh, J., Upadhyaya, C.P., Nookaraju, A., Pandey, S.K., & Park, S.W. (2012) Plant disease resistance genes: current status and future directions. Physiological and Molecular Plant Pathology, 78, 51-65 Abstract:
Plant diseases can drastically abate the crop yields as the degree of disease outbreak is getting severe around the world. Therefore, plant disease management has always been one of the main objectives of any crop improvement program. Plant disease resistance (R) genes have the ability to detect a pathogen attack and facilitate a counter attack against the pathogen. Numerous plant R-genes have been used with varying degree of success in crop improvement programs in the past and many of them are being continuously exploited. With the onset of recent genomic, bioinformatics and molecular biology techniques, it is quite possible to tame the R-genes for efficiently controlling the plant diseases caused by pathogens. This review summarizes the recent applications and future potential of R-genes in crop disease management.
Finally, this article takes a wider look at anti-viral mechanisms in plants, and discusse how innate immunity and RNA silencing act together to defend plants against viruses and other pathogens:
Zvereva, A.S., & Pooggin, M.M. (2012) Silencing and innate immunity in plant defense against viral and non-viral pathogens. Viruses, 4(11), 2578-2597 Abstract:
The frontline of plant defense against non-viral pathogens such as bacteria, fungi and oomycetes is provided by transmembrane pattern recognition receptors that detect conserved pathogen-associated molecular patterns (PAMPs), leading to pattern-triggered immunity (PTI). To counteract this innate defense, pathogens deploy effector proteins with a primary function to suppress PTI. In specific cases, plants have evolved intracellular resistance (R) proteins detecting isolate-specific pathogen effectors, leading to effector-triggered immunity (ETI), an amplified version of PTI, often associated with hypersensitive response (HR) and programmed cell death (PCD). In the case of plant viruses, no conserved PAMP was identified so far and the primary plant defense is thought to be based mainly on RNA silencing, an evolutionary conserved, sequence-specific mechanism that regulates gene expression and chromatin states and represses invasive nucleic acids such as transposons. Endogenous silencing pathways generate 21-24 nt small (s)RNAs, miRNAs and short interfering (si)RNAs, that repress genes post-transcriptionally and/or transcriptionally. Four distinct Dicer-like (DCL) proteins, which normally produce endogenous miRNAs and siRNAs, all contribute to the biogenesis of viral siRNAs in infected plants. Growing evidence indicates that RNA silencing also contributes to plant defense against non-viral pathogens. Conversely, PTI-based innate responses may contribute to antiviral defense. Intracellular R proteins of the same NB-LRR family are able to recognize both non-viral effectors and avirulence (Avr) proteins of RNA viruses, and, as a result, trigger HR and PCD in virus-resistant hosts. In some cases, viral Avr proteins also function as silencing suppressors. We hypothesize that RNA silencing and innate immunity (PTI and ETI) function in concert to fight plant viruses. Viruses counteract this dual defense by effectors that suppress both PTI-/ETI-based innate responses and RNA silencing to establish successful infection.