The article reviews the regulation and functions of the NLRP3 inflammasome in RNA virus infections. The NLRP3 inflammasome, composed of NLRP3, caspase-1, and ASC, plays a crucial role in innate immune responses by activating proinflammatory cytokines such as IL-1β and IL-18. The activation of the NLRP3 inflammasome involves two steps: priming and activation. Priming is initiated by pattern recognition receptors (PRRs) and involves the NF-κB pathway, leading to the transcription of pro-IL-1β and NLRP3. Activation is triggered by pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), resulting in the assembly and activation of the NLRP3 inflammasome, which activates caspase-1 and releases mature IL-1β. The article discusses the activation of the NLRP3 inflammasome by various RNA viruses, including positive-sense single-stranded RNA viruses (such as coronaviruses, flaviviruses, and enteroviruses), negative-sense single-stranded RNA viruses (such as influenza virus, Ebola virus, and respiratory syncytial virus), and double-stranded RNA viruses (such as reovirus). It highlights the mechanisms by which these viruses activate the NLRP3 inflammasome, including the involvement of viral proteins, signaling pathways, and cellular components. The clinical significance of NLRP3 inflammasome activation in viral diseases is also explored, emphasizing its role in disease severity and the potential for therapeutic strategies targeting the NLRP3 inflammasome to reduce inflammation and improve outcomes. Therapeutic approaches discussed include the use of cannabidiol, statins, berberine, probenecid, AZ11645373, ERK and NF-κB inhibitors, and disulfiram (DSF) to modulate the NLRP3 inflammasome and reduce inflammation during virus infections.The article reviews the regulation and functions of the NLRP3 inflammasome in RNA virus infections. The NLRP3 inflammasome, composed of NLRP3, caspase-1, and ASC, plays a crucial role in innate immune responses by activating proinflammatory cytokines such as IL-1β and IL-18. The activation of the NLRP3 inflammasome involves two steps: priming and activation. Priming is initiated by pattern recognition receptors (PRRs) and involves the NF-κB pathway, leading to the transcription of pro-IL-1β and NLRP3. Activation is triggered by pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), resulting in the assembly and activation of the NLRP3 inflammasome, which activates caspase-1 and releases mature IL-1β. The article discusses the activation of the NLRP3 inflammasome by various RNA viruses, including positive-sense single-stranded RNA viruses (such as coronaviruses, flaviviruses, and enteroviruses), negative-sense single-stranded RNA viruses (such as influenza virus, Ebola virus, and respiratory syncytial virus), and double-stranded RNA viruses (such as reovirus). It highlights the mechanisms by which these viruses activate the NLRP3 inflammasome, including the involvement of viral proteins, signaling pathways, and cellular components. The clinical significance of NLRP3 inflammasome activation in viral diseases is also explored, emphasizing its role in disease severity and the potential for therapeutic strategies targeting the NLRP3 inflammasome to reduce inflammation and improve outcomes. Therapeutic approaches discussed include the use of cannabidiol, statins, berberine, probenecid, AZ11645373, ERK and NF-κB inhibitors, and disulfiram (DSF) to modulate the NLRP3 inflammasome and reduce inflammation during virus infections.