| Literature DB >> 24418550 |
Megan E Ermler1, Zachary Traylor2, Krupen Patel2, Stefan A Schattgen3, Sivapriya K Vanaja3, Katherine A Fitzgerald3, Amy G Hise4.
Abstract
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-1β 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-1β during infection. Finally, direct imaging using confocal microscopy shows that the MAVS protein co-localizes with NLRP3 in the cytoplasm of RVFV infected cells.Entities:
Keywords: ASC; Caspase-1; Dendritic cells; IL-1β; Inflammasome; Murine; NLRP3; Rift Valley fever virus; Virus
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Year: 2013 PMID: 24418550 PMCID: PMC3951897 DOI: 10.1016/j.virol.2013.11.015
Source DB: PubMed Journal: Virology ISSN: 0042-6822 Impact factor: 3.616