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Abstract

Viruses that cause economically important diseases spread systemically in the plant. However, in several laboratory test or indicator plants, the virus after multiplying in several hundred cells around the point of entry, does not continue to spread and remains in a local infection. Several types of local infections are known (Loebenstein et al. 1982): (a) self-limiting necrotic local lesions such as Tobacco mosaic virus (TMV) in Datura strammonium, where lesions reach their maximum size three days after inoculation; (b) chlorotic local lesions, such as Potato virus Y (PVY) in Chenopodium amaranticolor, where infected cells lose chlorophyll; (c) ring-like patterns or ringspots that remain localized, such as Tetragonia expansa infected with Tomato spotted wilt virus (TSWV); (d) starch lesions, such as TMV in cucumber cotyledons, where no symptoms are observed on the intact leaf, but when it is decolorized with ethanol and stained with iodine, lesions become apparent; (e) microlesions (with a mean size of 1.1 x 10−2 mm2), such as the U2 of TMV on Pinto bean leaves; and (f) subliminal symptomless infections not detectable as starch lesions., as in TMV-infected cotton cotyledons, where virus content is 1/200,000 of that produced in a systemic host (Cheo, 1970). The localized infection is an efficient mechanism whereby plants resist viruses, though most viral resistance genes are not associated with the hypersensitive response (HR), but affect virus multiplication or movement as a result of incompatible viral and host factors.

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Loebenstein, G., Akad, F. (2006). The Local Lesion Response. In: Loebenstein, G., Carr, J.P. (eds) Natural Resistance Mechanisms of Plants to Viruses. Springer, Dordrecht. https://doi.org/10.1007/1-4020-3780-5_5

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