Inflammasomes are macromolecular multiprotein complexes that exist in the cytoplasm and participate in innate immune defense. They are activated under infection or stress, triggering the release of pro-inflammatory cytokines such as IL-1β and IL-18 and inducing pyroptosis. NLRP3 recognizes various pathogen-associated molecular patterns (PAMP) and danger-associated molecular patterns (DAMP) produced during virus replication, which initiates the NLRP3 inflammasome-dependent antiviral immune response. However, some viruses have evolved complex strategies to evade innate immune surveillance by targeting inflammasomes. IL-1β has profound influence on host immune response to viral infections. Besides, the activation of inflammasome is imperative in the maturation of IL-1β. Therefore, inflammasome is a potential target for both the host and viruses to regulate immune responses. Here, we discuss the crosstalk between the NLRP3 inflammasome and viruses, providing an overview of viral infection-induced NLRP3 inflammasome activation, and the immune escape strategies of viruses through modulating the NLRP3 inflammasome activity.