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Look Who’s Talking: T-Even Phage Lysis Inhibition the Granddaddy of Virus-Virus Intercellular Communication Research

机译:看看谁在说话:T-Even噬菌体抑制作用病毒-病毒细胞间通讯研究的祖父

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摘要

That communication can occur between virus-infected cells has been appreciated for nearly as long as has virus molecular biology. The original virus communication process specifically was that seen with T-even bacteriophages—phages T2, T4, and T6—resulting in what was labeled as a lysis inhibition. Another proposed virus communication phenomenon, also seen with T-even phages, can be described as a phage-adsorption-induced lysis-inhibition collapse. Both are mediated by virions that were released from earlier-lysing, phage-infected bacteria. Each may represent ecological responses, in terms of phage lysis timing, to high local densities of phage-infected bacteria, but for lysis inhibition also to locally reduced densities of phage-uninfected bacteria. With lysis inhibition, the outcome is a temporary avoidance of lysis, i.e., a lysis delay, resulting in increased numbers of virions (greater burst size). Synchronized lysis-inhibition collapse, by contrast, is an accelerated lysis which is imposed upon phage-infected bacteria by virions that have been lytically released from other phage-infected bacteria. Here I consider some history of lysis inhibition, its laboratory manifestation, its molecular basis, how it may benefit expressing phages, and its potential ecological role. I discuss as well other, more recently recognized examples of virus-virus intercellular communication.
机译:几乎可以与病毒分子生物学一样早就认识到可以在病毒感染的细胞之间发生通信。具体而言,最初的病毒传播过程是通过T-even噬菌体(噬菌体T2,T4和T6)看到的,导致了裂解抑制作用。另一个建议的病毒传播现象,也与T-even噬菌体一起出现,可以描述为噬菌体吸附诱导的裂解抑制崩溃。两者均由从较早裂解的噬菌体感染的细菌释放的病毒粒子介导。就噬菌体裂解时间而言,每一种都可以代表对噬菌体感染细菌的高局部密度的生态响应,但是对于裂解抑制,对于噬菌体未感染细菌的局部降低的密度也可以表示为生态响应。具有裂解抑制作用,其结果是暂时避免裂解,即裂解延迟,导致病毒体数目增加(更大的爆发大小)。相比之下,同步裂解抑制崩溃是一种加速裂解,它是由已经从其他噬菌体感染的细菌中裂解释放出的病毒体施加到噬菌体感染的细菌上的。在这里,我考虑了裂解抑制作用的历史,其实验室表现,其分子基础,它可能如何有益于表达噬菌体及其潜在的生态作用。我还讨论了病毒-病毒细胞间通讯的其他最近认可的例子。

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