Hendra virus is an emerging virus with a geographically broad host reservoir capable of infecting a variety of hosts. In humans, Hendra virus causes overt inflammatory disease of the lung and nervous system driven in part by the inflammatory cytokine IL-1β. There are currently no therapeutic options available for patients who contract Hendra virus, and very little of how it induces inflammatory disease is currently known. Recent studies have identified viral aggregating proteins as drivers of inflammation in Influenza A virus and SARS-Cov-2 virus. In this study, we sought to identify mechanisms of inflammation during Hendra virus infection and the possibility of another viral aggregating protein driving inflammatory disease. We have shown that a peptide analogue of Hendra virus C protein is able to form protein aggregates and activate the NLRP3 inflammasome through phagocytic uptake into cells in vitro using both temporal inhibition and gene deletion. Treatment of cells with the NLRP3 inhibitor MCC950 ameliorated IL-1β secretion responses, highlighting a possible therapeutic angle to reduce inflammation during Hendra virus infections. These results demonstrate a possible contributor of the detrimental immunopathology identified in Hendra virus infections, and critically identify a possible therapeutic strategy to alleviate inflammatory disease in infected patients.