PubMed2001
Cross protection is a type of induced resistance developing in plants against viruses. Its basis is that prior infection with one virus affords protection against closely related ones. Its history started about seventy years ago, when the Dutchman Thung and the Englishman Salaman described the phenomenon independently. During the 1930s, several virologists confirmed the discovery, which was considered the first possibility to protect plants against virus infection. Growing interest also led plant virologists to formulate the first hypotheses on its mechanism, with the onset of a still unsolved debate. The hypotheses, that have been succeeded until the 1970s, included (i) antibody formation, (ii) exhaustion of essential metabolites, (iii) limited sites for virus multiplication, and (iv) specific adsorption by new cell compounds. These hypotheses were re-proposed and discussed on several occasions without arriving at a final conclusion. The statement of molecular genetics of viruses produced new interesting "theories", fundamentally based on the interference between virus strains. A model developed by the Americans Palukaitis and Zaitlin in 1984 indicates that excess of progeny positive-sense RNA of the protecting strain would sequester the minus-strand RNA of the challenging strain. Other models involve a function of the coat protein, or gene recombination. However, no model that could unify all the various facets of cross protection has hitherto been proposed. All that has not stopped the phenomenon having practical application. From the first attempts against a severe disease of cocoa in West Africa realized by Posnette in the 1940s, a number of crops (such as tomato, tobacco, citrus, cucurbits, grapevine, soybean, papaya, and so on) have been submitted to this practice. During the 1980s, cross protection came to a standstill because of the development of new resistant or tolerant cultivars. Its story is by no means ended, and much work is needed to understand its limits and possibilities.