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The Induction of IL-1β Secretion Through the NLRP3 Inflammasome During Ebola Virus Infection
Author(s) -
Peter Halfmann,
Lindsay Hill-Batorski,
Yoshihiro Kawaoka
Publication year - 2018
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1093/infdis/jiy433
Subject(s) - inflammasome , proinflammatory cytokine , ebola virus , secretion , innate immune system , caspase 1 , pyroptosis , immunology , inflammation , pathogenesis , immune system , biology , virus , virology , biochemistry
The inflammasome is part of the innate immune system that regulates the secretion of proinflammatory cytokines such as interleukin-1β (IL-1β). Ebola virus (EBOV) infection of monocytes and macrophages (primary target cells early during infection) leads to the production of proinflammatory cytokines; however, the mechanism behind the activation and release of these cytokines is not fully understood. Here, we demonstrate that EBOV infection leads to the activation of the NLRP3 inflammasome and the subsequent secretion of IL-1β and IL-18. This process is dependent on protease caspase-1, a component of the NLRP3 inflammasome complex, but is independent of virus replication. These findings may lead to the development of novel drugs that impede the pathogenesis of EBOV infection.

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