Rift Valley fever virus infection induces activation of the NLRP3 inflammasome
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Authors
Ermler, Megan E.Traylor, Zachary
Patel, Krupen
Schattgen, Stefan A.
Vanaja, Sivapriya K.
Fitzgerald, Katherine A.
Hise, Amy G.
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyDocument Type
Journal ArticlePublication Date
2014-01-20Keywords
Adaptor Proteins, Signal TransducingAnimals
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
Metadata
Show full item recordAbstract
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.Source
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 siteDOI
10.1016/j.virol.2013.11.015Permanent Link to this Item
http://hdl.handle.net/20.500.14038/34963PubMed ID
24418550Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.virol.2013.11.015