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Virology. 2014 Jan 20;449:174-80. doi: 10.1016/j.virol.2013.11.015. Epub 2013 Dec 3.

Rift Valley fever virus infection induces activation of the NLRP3 inflammasome.

Author information

1
Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH, USA.
2
Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106, USA.
3
Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA.
4
Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH, USA; Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, OH, USA. Electronic address: amy.hise@case.edu.

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.

KEYWORDS:

ASC; Caspase-1; Dendritic cells; IL-1β; Inflammasome; Murine; NLRP3; Rift Valley fever virus; Virus

PMID:
24418550
PMCID:
PMC3951897
DOI:
10.1016/j.virol.2013.11.015
[Indexed for MEDLINE]
Free PMC Article
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