Publisher Summary The RNA phages indeed deserve to be considered among the “living world.” They possess well-developed powers of genetic regulation, morphogenesis, chromosomal replication, and even adaptation. In the broadest sense the virus must use all of its genetic and chemical potential, while making maximal use of existing host reactions. In other words, by prudent use of its chemical potential these tiny phages have achieved the “living” state with far fewer genes than higher organisms. The viral proteins themselves are highly versatile in function, and it seems clear that studies directed toward understanding the functional nature of a given viral protein will lead to the discovery of multiple “active sites” on the protein. The tiny RNA chromosome, itself a functional partner in many of these reactions, must also be graced with a multitude of “active sites.” These sites behave as special genetic elements and function, for example, as adsorption points for viral polymerase or capsid as repressor. These sites give the chromosome a type of communication system with the cytoplasm. In one case, a chromosome-cytoplasm circuit of communication is achieved when the capsid protein locks on the chromosome, and switches off the polymerase at a certain time in the infective cycle. This feedback circuit using capsid, itself a product of the infection, endows the virus with powers of self-regulation. The initiation of the RNA replication cycle may require an even more sophisticated protein-chromosome interaction, one where the polymerase is forced to seek out a single parental molecule to use as template among a variety of different host RNA species. When this union is achieved, the infection switches from a purely translational state to the transcriptional cycle where many more copies of RNA are made. The chromosome then appears to monitor the work of the infection going on around it through this form of communication.