Significance Probabilistic bet hedging is a generalized diversification strategy to maximize fitness in unpredictable environments and has been proposed as an evolutionary basis for herpesvirus latency. However, the molecular mechanisms enabling probabilistic bet hedging have remained elusive. Here, we find that the human herpesvirus cytomegalovirus—a major cause of birth defects and transplant failures—utilizes stochastic variability in the abundance of a protein packaged into individual viral particles to enable probabilistic bet hedging between alternate viral states.