Infection causes reduced activity, anorexia, and sleep, which are components of the phylogenetically conserved but poorly-understood sickness behavior. We developed a C. elegans model to study quiescence during chronic infection, using infection with the Orsay virus. The Orsay virus infects intestinal cells yet strongly affects behavior, indicating gut-to-nervous system communication. Infection quiescence has the sleep properties of reduced responsiveness and rapid reversibility. Both the ALA and RIS neurons regulate virus-induced quiescence though ALA plays a more prominent role. Quiescence-defective animals have decreased survival when infected, indicating a benefit of quiescence during chronic infectious disease. The survival benefit of quiescence is not explained by a difference in viral load, indicating that it improves resilience rather than resistance to infection. Orsay infection is associated with a decrease in ATP levels, and this decrease is more severe in quiescence-defective animals. We propose that quiescence preserves energetic resources by reducing energy expenditures and/or by increasing extraction of energy from nutrients. This model presents an opportunity to explore the role of sleep and fatigue in chronic infectious illness.Significance statement Sleepiness and fatigue are cardinal symptoms of infectious disease. We do not understand the mechanisms regulating sleep during sickness, how sickness sleep differs from regular sleep, and whether sickness sleep is beneficial to recovery from illness. We present a model for studying sleep-like quiescence during viral infection in the roundworm C. elegans Sickness quiescence in worms relies on different neural circuitry than other forms of sleep. Quiescence during viral infection increases survival by improving resilience. Loss of quiescence during sickness leads to a drop in ATP levels, suggesting that it improves survival by conserving energy.