Abstract
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 synchronized 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.
Highlights
That communication can occur between virus-infected cells has been appreciated for nearly as long as has virus molecular biology
If it is extracellular lysozyme that is responsible for the larger size of T4 wild-type plaques following chloroform-vapor treatment (Figure 3), we would expect, for example, that r mutant plaques would be readily able to invade the chloroform-clearable areas of a wild-type plaque
Equivalent colliding-plaque observations can be seen in the plaque photographs presented by Hershey and Rotman [78], which are based on phage T2H and E. coli strain S; see Hershey [65] as well as Lanni [79]
Summary
“ . . . the earliest genetic analyses of phage biology centered on the study of lysis inhibition (LIN). Both involve delays in phage-induced bacterial lysis Both involve, at least in principle, these systems differ in that one is displayed within a context of temperate phages and resulting an increase in the number of phages produced by signal-receiving phage-infected bacteria [11,12]. An additional mechanism of virion-mediated, virus-virus intercellular communication phages [17], was dubbed a lysis-inhibition collapse,possible and a synchronized. Lysis inhibition results in an extended primary infection lytic cycle and resulting increase in infection burst size; LIN is an example of phage-associated intercellularly mediated communication. A mechanism (mechanism 2) potentially underlying certain aspects of lysis-inhibition (LIN) collapse, unsynchronized LIN Such as might be caused by excessive lysis from without- (LO-) like secondary adsorption-associated damage to otherwise lysis-inhibited (LINed) bacteria infected with sp or imm mutant phages. See lysis-inhibition (LIN) collapse proposed mechanisms 1 and 2; contrast with synchronized lysis-inhibition (LIN) collapse
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