Plants are infected by a huge number ofpathogens of which only a few succeed in causing disease. The attack by othersis responded by a sophisticated immune system possessed by the plants.
Entry ofphytopathogen is a vital step in causing disease. Especially in viral infection, entry ispossibly through physical injuries induced either by environmental factors orby vectors like whiteflies in the case of geminivirus infection (Niehl andHeinlein 2010). Once the virus enters into the plant cell, it mobilizes locally and systematically through intracellularmovement through the plasmodesmata. As a counter defense, plants have inbuiltimmune system like microbial-associated molecular-patterns-triggered immunity(MTI) and effector-triggered immunity (ETI). MTI confers basal resistance,while ETI confers durable resistance, often resulting in hypersensitiveresponse. Precisely, MTI involves the recognition of microbial elicitors calledmicrobial-associated molecular patterns (MAMPs) (oligogalacturonides,ergosterol, bacterial flagellin, xylanase, chitin, cold-shock protein, cellwall fragments, peptides, and lipopolysaccharides) by a class ofplasma-membrane-bound extracellular receptors called pattern recognitionreceptors (PRRs) (Dodds and Rathjen 2010; Beck et al.
2012) and the activationof these PRRs results in active defense responses (Hammond-Kosack and Jones1996), which ultimately contribute to stop the progress of infection before themicrobe gains a hold in the plant. Pathogens that escapes from MTI aresubjected to ETI in which pathogens ejects huge numbers of effector proteinsinto the cytoplasm of infected plant cells. These effector molecules arerecognized by plant disease resistant (R) genes. The protein of R genes hasnucleotide binding leucine repeat (NB-LRR) which bind to the effector moleculesand controls the plant-pathogen interactions in a variety of host against anextensive list of pathogens (Martin et al.
2003). In the later ETI response activatesdownstream MAPK cascade and WRKY transcription factors. This subsequentlyinduces rapid transcriptional activation of a string of pathogenesis-related(PR) genes in and around the infected cell for the biosynthesis of salicylicacid (SA), jasmonic acid (JA), ethylene (ET), cell wall strengthening,lignifications, production of various antimicrobial compounds in endoplasmicreticulum and secretion into vacuoles (Iwai et al. 2006; Nomura et al. 2012;Schäfer and Eichmann 2012).
Salicylic acid thus accumulated in the infectedareas binds to the receptor NPR3 (NONEXPRESSOR OF PR GENES3) with low affinityand mediates the degradation of cell-death suppressor NPR1 (Fu et al. 2012),thus leading to the development of hypersensitive response (HR) (Pennell andLamb 1997; Hayward et al. 2009). The HR is a form of programmed cell death(PCD) characterized by cytoplasmic shrinkage, chromatin condensation,mitochondrial swelling, vacuolization and chloroplast disruption (Coll et al.2011). Plants also possess systemic acquired resistance (SAR), which provideslong-term defense against a broad-spectrum of pathogens.
In addition, plants encounterthe viral infection through RNA interference phenomena by utilizing small RNAs.