Rift Valley fever virus infection induces activation of the NLRP3 inflammasome
Department of Medicine, Division of Infectious Diseases and Immunology
Adaptor Proteins, Signal Transducing; Animals; Carrier Proteins; Caspase 1; Dendritic Cells; Female; Humans; Inflammasomes; Interleukin-1beta; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Rift Valley Fever; Rift Valley fever virus
Amino Acids, Peptides, and Proteins | Cells | Immunity | Immunology and Infectious Disease | Immunology of Infectious Disease | Infectious Disease | Molecular Genetics | Virology | Virus Diseases | Viruses
Inflammasome activation is gaining recognition as an important mechanism for protection during viral infection. Here, we investigate whether Rift Valley fever virus, a negative-strand RNA virus, can induce inflammasome responses and IL-1beta processing in immune cells. We have determined that RVFV induces NLRP3 inflammasome activation in murine dendritic cells, and that this process is dependent upon ASC and caspase-1. Furthermore, absence of the cellular RNA helicase adaptor protein MAVS/IPS-1 significantly reduces extracellular IL-1beta during infection. Finally, direct imaging using confocal microscopy shows that the MAVS protein co-localizes with NLRP3 in the cytoplasm of RVFV infected cells.
DOI of Published Version
Virology. 2014 Jan 20;449:174-80. doi: 10.1016/j.virol.2013.11.015. Epub 2013 Dec 3. Link to article on publisher's site
Ermler ME, Traylor Z, Patel K, Schattgen SA, Vanaja SK, Fitzgerald KA, Hise AG. (2014). Rift Valley fever virus infection induces activation of the NLRP3 inflammasome. Infectious Diseases and Immunology Publications. https://doi.org/10.1016/j.virol.2013.11.015. Retrieved from https://escholarship.umassmed.edu/infdis_pp/184