The magnitude of an epidemic depends on host susceptibility to the disease, a trait influenced by the genetic constitution of the host and its environment. While the genetic basis of disease susceptibility is often associated with immune capacities, environmental effects generally reflect complex physiological trade-offs. We suggest here that in the case of obligate pathogens whose proliferation depends on the cellular machinery of the host (e.g. viruses), disease susceptibility is directly influenced by host growth. To test our hypothesis, we focussed on a viral disease affecting an ecologically relevant model exploited worldwide, the Pacific oyster Crassostrea gigas. Oysters originating from 3 lines with contrasting resistance to the disease were divided into 3 groups displaying different growth rates and acclimated to 3 food levels and 2 temperatures to generate different growth rates. These oysters were then exposed to the virus, and survival and viral shedding were measured. Finally, we developed a risk model to rank the relative importance of temperature, food, genetic selection and growth on disease-induced mortality. We found that increasing growth through temperature, food level or selection of fast-growing animals all increased mortality, especially in host populations where susceptible phenotypes dominated. Food provisioning was the most influential factor associated with higher viral shedding, followed by temperature, resistance phenotype and growth rate. We suggest that growth-forcing factors may promote the development of obligate intracellular pathogens and epidemic risk, thus opening up avenues for disease management based on the manipulation of host metabolism.