Pennazio S, Roggero P, Conti M
Istituto di Fitovirologia applicata del CNR, Torino, Italy.
New Microbiol. 2001 Jan;24(1):99-114.
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.
交叉保护是植物中产生的一种针对病毒的诱导抗性。其基础是先前感染一种病毒可提供针对密切相关病毒的保护。其历史始于约七十年前，当时荷兰人通和英国人萨拉曼独立描述了这一现象。在20世纪30年代，几位病毒学家证实了这一发现，这被认为是保护植物免受病毒感染的第一种可能性。日益增长的兴趣也促使植物病毒学家就其机制提出了第一批假说，引发了一场至今仍未解决的争论。直到20世纪70年代一直成功的假说包括：（i）抗体形成；（ii）必需代谢物的耗尽；（iii）病毒繁殖的有限位点；以及（iv）新细胞化合物的特异性吸附。这些假说被多次重新提出并讨论，但没有得出最终结论。病毒分子遗传学的阐述产生了新的有趣“理论”，这些理论基本上基于病毒株系之间的干扰。1984年美国人帕卢凯蒂斯和扎伊特林开发的一个模型表明，保护株系的子代正义RNA过量会隔离挑战株系的负链RNA。其他模型涉及衣壳蛋白的功能或基因重组。然而，迄今为止还没有一个模型能够统一交叉保护的所有不同方面。所有这些都没有阻止这一现象得到实际应用。从20世纪40年代波斯内特针对西非可可的一种严重病害进行的首次尝试开始，许多作物（如番茄、烟草、柑橘、葫芦科植物、葡萄、大豆、木瓜等）都采用了这种做法。在20世纪80年代，由于新的抗性或耐受性品种的开发，交叉保护陷入停滞。它的故事远未结束，还需要做很多工作来了解其局限性和可能性。
