Chapter title |
Roles of Arenavirus Z Protein in Mediating Virion Budding, Viral Transcription-Inhibition and Interferon-Beta Suppression
|
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Chapter number | 16 |
Book title |
Hemorrhagic Fever Viruses
|
Published in |
Methods in molecular biology, January 2018
|
DOI | 10.1007/978-1-4939-6981-4_16 |
Pubmed ID | |
Book ISBNs |
978-1-4939-6980-7, 978-1-4939-6981-4
|
Authors |
Junjie Shao, Yuying Liang, Hinh Ly |
Abstract |
The smallest arenaviral protein is the zinc-finger protein (Z) that belongs to the RING finger protein family. Z serves as a main component required for virus budding from the membrane of the infected cells through self-oligomerization, a process that can be aided by the viral nucleoprotein (NP) to form the viral matrix of progeny virus particles. Z has also been shown to be essential for mediating viral transcriptional repression activity by locking the L polymerase onto the viral promoter in a catalytically inactive state, thus limiting viral replication. The Z protein has also recently been shown to inhibit the type I interferon-induction pathway by directly binding to the intracellular pathogen-sensor proteins RIG-I and MDA5, and thus inhibiting their normal functions. This chapter describes several assays used to examine the important roles of the arenaviral Z protein in mediating virus budding (i.e., either Z self-budding or NP-Z budding activities), viral transcriptional inhibition in a viral minigenome (MG) assay, and type I IFN suppression in an IFN-β promoter-mediated luciferase reporter assay. |
Mendeley readers
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Demographic breakdown
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Other | 1 | 5% |
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