The NLRP3 inflammasome is a key component of the innate immune system that plays a critical role in the host's response to viral infections. It is composed of three main components: NLRP3, ASC, and caspase-1. Upon activation, the NLRP3 inflammasome triggers caspase-1 to induce pyroptosis, a form of programmed cell death, which leads to the maturation and secretion of pro-inflammatory cytokines such as IL-1β and IL-18. These cytokines are essential for the immune response against viral infections. However, the activation of the NLRP3 inflammasome can also be inhibited by certain viruses, which may contribute to viral pathogenesis. RNA viruses, including coronaviruses, flaviviruses, enteroviruses, retroviruses, influenza viruses, Ebola viruses, respiratory syncytial viruses, Rift Valley Fever viruses, and hantaviruses, have been shown to interact with the NLRP3 inflammasome in various ways. Some viruses activate the NLRP3 inflammasome, leading to the production of inflammatory cytokines, while others inhibit its activation, potentially reducing the host's immune response. The mechanisms by which these viruses regulate the NLRP3 inflammasome involve various pathways, including the activation of signaling pathways such as NF-κB, the production of reactive oxygen species (ROS), and the release of ions such as calcium and potassium. The regulation of the NLRP3 inflammasome by RNA viruses is a complex process that involves multiple cellular events. The activation of the NLRP3 inflammasome can be divided into two steps: signal 1, which primes the inflammasome, and signal 2, which activates it. Signal 1 involves the activation of the NF-κB pathway, leading to the transcription of pro-inflammatory cytokines such as IL-1β and IL-18. Signal 2 involves the activation of the NLRP3 inflammasome by various stimuli, including viral particles, proteins, and nucleic acids. The clinical significance of NLRP3 inflammasome activation in viral diseases is significant. The activation of the NLRP3 inflammasome can lead to the production of inflammatory cytokines, which can contribute to the severity of viral infections. However, the activation of the NLRP3 inflammasome can also be a target for therapeutic strategies aimed at reducing inflammation in viral infections. Targeting the NLRP3 inflammasome or its associated cytokines such as IL-1β may provide a promising approach for the treatment of viral infections.The NLRP3 inflammasome is a key component of the innate immune system that plays a critical role in the host's response to viral infections. It is composed of three main components: NLRP3, ASC, and caspase-1. Upon activation, the NLRP3 inflammasome triggers caspase-1 to induce pyroptosis, a form of programmed cell death, which leads to the maturation and secretion of pro-inflammatory cytokines such as IL-1β and IL-18. These cytokines are essential for the immune response against viral infections. However, the activation of the NLRP3 inflammasome can also be inhibited by certain viruses, which may contribute to viral pathogenesis. RNA viruses, including coronaviruses, flaviviruses, enteroviruses, retroviruses, influenza viruses, Ebola viruses, respiratory syncytial viruses, Rift Valley Fever viruses, and hantaviruses, have been shown to interact with the NLRP3 inflammasome in various ways. Some viruses activate the NLRP3 inflammasome, leading to the production of inflammatory cytokines, while others inhibit its activation, potentially reducing the host's immune response. The mechanisms by which these viruses regulate the NLRP3 inflammasome involve various pathways, including the activation of signaling pathways such as NF-κB, the production of reactive oxygen species (ROS), and the release of ions such as calcium and potassium. The regulation of the NLRP3 inflammasome by RNA viruses is a complex process that involves multiple cellular events. The activation of the NLRP3 inflammasome can be divided into two steps: signal 1, which primes the inflammasome, and signal 2, which activates it. Signal 1 involves the activation of the NF-κB pathway, leading to the transcription of pro-inflammatory cytokines such as IL-1β and IL-18. Signal 2 involves the activation of the NLRP3 inflammasome by various stimuli, including viral particles, proteins, and nucleic acids. The clinical significance of NLRP3 inflammasome activation in viral diseases is significant. The activation of the NLRP3 inflammasome can lead to the production of inflammatory cytokines, which can contribute to the severity of viral infections. However, the activation of the NLRP3 inflammasome can also be a target for therapeutic strategies aimed at reducing inflammation in viral infections. Targeting the NLRP3 inflammasome or its associated cytokines such as IL-1β may provide a promising approach for the treatment of viral infections.