Plants are infected by a large number of pathogens, of which only a few can cause disease. A sophisticated immune system possessed by plants responds to the attack of others. Entry of the phytopathogen is a critical step in causing the disease. Especially in viral infection, entry probably occurs through physical injury induced by environmental factors or by vectors such as whiteflies in the case of geminivirus infection (Niehl and Heinlein 2010). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Once the virus enters the plant cell, it mobilizes locally and systemically through intracellular movement through the plasmodesmata. As a counterdefense, plants have a built-in immune system such as microbe-associated molecular pattern-triggered immunity (MTI) and effector-triggered immunity (ETI). MTI confers basal resistance, whereas ETI confers long-lasting resistance, often resulting in a hypersensitive response. Precisely, MTI involves the recognition of microbial elicitors called microbial-associated molecular patterns (MAMPs) (oligogalacturonides, ergosterol, bacterial flagellin, xylanase, chitin, cold shock protein, cell wall fragments, peptides and lipopolysaccharides) by a class of membrane-bound extracellular receptors called pattern recognition receptors (PRRs) (Dodds and Rathjen 2010; Beck et al. 2012), and activation of these PRRs results in active defense responses (Hammond-Kosack and Jones 1996) , which ultimately help stop the progress of the infection before the microbe establishes itself in the plant. Pathogens escaping from the MTI undergo ETI in which the pathogens excrete massive numbers of effector proteins into the cytoplasm of infected plant cells. These effector molecules are recognized by plant disease resistance (R) genes. The R gene protein has nucleotide-binding leucine repeats (NB-LRRs) that bind to effector molecules and control plant-pathogen interactions in a variety of hosts against an extensive list of pathogens (Martin et al. 2003). The ETI response activates the downstream MAPK cascade and WRKY transcription factors. This subsequently induces rapid transcriptional activation of a series of pathogenesis-related (PR) genes in and around the infected cell for the biosynthesis of salicylic acid (SA), jasmonic acid (JA), ethylene (ET ), cell wall strengthening, lignifications, production of various antimicrobial compounds in the endoplasmic reticulum, and secretion into vacuoles (Iwai et al. 2006; Nomura et al. 2012; Schäfer and Eichmann 2012). The salicylic acid thus accumulated in the infected areas binds to the NPR3 (NONEXPRESSOR OF PR GENES3) receptor with low affinity and mediates the degradation of the cell death suppressor NPR1 (Fu et al. 2012), thus leading to the development of a hypersensitive response ( HR ) (Pennell and Lamb 1997; Hayward et al. 2009). HR is a form of programmed cell death (PCD) characterized by cytoplasmic shrinkage, chromatin condensation, mitochondrial swelling, vacuolization, and chloroplast destruction (Coll et al. 2011). Please note: this is just an example. Get a custom paper from our expert writers now. Get a Custom Essay Plants also possess systemic acquired resistance (SAR), which provides long-term defense against a broad spectrum of pathogens. Furthermore, plants encounter viral infection through RNA interference phenomena using small RNAs.