Rift Valley fever virus infection induces activation of the NLRP3 inflammasome

UMMS Affiliation

Department of Medicine, Division of Infectious Diseases and Immunology

Publication Date


Document Type



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

Journal/Book/Conference Title


Related Resources

Link to Article in PubMed

PubMed ID