We are interested in expanding models of virus-host interactions across the symbiosis continuum from antagonism to mutualism. We describe a novel mechanism of viral maintenance through infection-induced dormancy and death. We demonstrate that, through this mechanism, virus infection changes cells into killer archaea that out-compete uninfected cells to extinction. Based on the distribution of CRISPR-cas sequences we hypothesize that this mechanism evolved to evade CRISPR-cas immunity. Combining investigations of natural variation with phenotypic characterization in experimental evolution, we identify trade-offs associated with infection, immunity, defense and antagonism in this system and provide insight into the evolutionary path that results in maintenance of diversity of interactions in virus-host symbiosis.