About: CRISPR/Cas9 knockout of USP18 enhances type I IFN responsiveness and restricts HIV-1 infection in macrophages

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About: CRISPR/Cas9 knockout of USP18 enhances type I IFN responsiveness and restricts HIV-1 infection in macrophages Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	CRISPR/Cas9 knockout of USP18 enhances type I IFN responsiveness and restricts HIV-1 infection in macrophages
Creator	Nakanishi, Mahito Terada, Naohiro Cash, Melanie Crispr, S Santostefano, Katherine Stat, Jak Taylor, Jared Wallet, Mark Y W O R D, K
Source	Medline; PMC
abstract	The IFN-stimulated gene ubiquitin specific proteinase 18 (USP18) encodes a protein that negatively regulates T1 IFN signaling via stearic inhibition of JAK1 recruitment to the IFNα receptor 2 subunit (IFNAR2). Here we demonstrate that USP18 expression is induced by HIV-1 in a T1 IFN dependent manner. Experimental depletion of USP18 by CRISPR/Cas9 gene editing results in a significant restriction of HIV-1 replication in an induced pluripotent stem cell (iPSC)-derived macrophage model. In the absence of USP18, macrophages have increased responsiveness to stimulation with T1 IFNs with prolonged phosphorylation of STAT1 and STAT2 and increased expression of interferon-stimulated genes that are key for antiviral responses. Interestingly, HIV-1 requires some signaling through the T1 IFN receptor to replicate efficiently because a neutralizing antibody that inhibits T1 IFN activity reduces HIV-1 replication rate in monocyte-derived macrophages. USP18 induction by HIV-1 tunes the IFN response to optimal levels allowing for efficient transcription from the HIV-1 LTR promoter while minimizing the T1 IFN-induced antiviral response that would otherwise restrict viral replication and spread. Finally, iPSC and CRISPR/Cas9 gene targeting offer a powerful tool to study host factors that regulate innate immune responses.
has issue date	2018-02-13(xsd:dateTime)
bibo:doi	10.1002/jlb.3mia0917-352r
bibo:pmid	29437254
has license	green-oa
sha1sum (hex)	4fb5e7fb5d3ec9366bfa98bb436d3b34dc4755fb
schema:url	https://doi.org/10.1002/jlb.3mia0917-352r
resource representing a document's title	CRISPR/Cas9 knockout of USP18 enhances type I IFN responsiveness and restricts HIV-1 infection in macrophages
has PubMed Central identifier	PMC6754309
has PubMed identifier	29437254
schema:publication	Journal of Leukocyte Biology
resource representing a document's body	covid:4fb5e7fb5d3ec9366bfa98bb436d3b34dc4755fb#body_text
is schema:about of	named entity 'HIV-1' named entity 'IFN' named entity 'derived' named entity 'CRISPR/Cas9' named entity 'inhibition' named entity 'proteinase' named entity 'type I IFN' named entity 'recruitment' named entity 'editing' named entity 'response' named entity 'macrophages' named entity 'innate immune responses' named entity 'iPSC' named entity 'signaling' named entity 'HIV-1' named entity 'demonstrate' named entity 'response' named entity 'encodes' named entity 'Here' named entity 'restrict' named entity 'protein' named entity 'ubiquitin' named entity 'macrophage' named entity 'receptor' named entity 'STAT2' named entity 'CRISPR' named entity 'USP18' named entity 'USP18' named entity 'protein' named entity 'macrophages' named entity 'JAK1' named entity 'siRNA' named entity 'apoptosis' named entity 'HIV-1' named entity 'T75' named entity 'USP18' named entity 'protease' named entity 'STAT1' named entity 'macrophages' named entity 'IFN' named entity 'STAT2' named entity 'iMacs' named entity 'HIV-1' named entity 'chronic disease' named entity 'antiviral' named entity 'antiviral' named entity 'ubiquitin-like' named entity 'induced expression' named entity 'phosphorylation' named entity 'JAK-STAT signaling' named entity 'cell line' named entity 'dose-dependent manner' named entity 'HIV-1' named entity 'recombinant' named entity 'cancer cells' named entity 'dose-dependent manner' named entity 'protein' named entity 'HIV-1' named entity 'gene editing' named entity 'ISG15' named entity 'USP18' named entity 'USP18' named entity 'USP18' named entity 'phosphorylation' named entity 'USP18' named entity 'CD68' named entity 'USP18' named entity 'Monocyte-derived macrophages' named entity 'viral replication' named entity 'macrophages' named entity 'USP18' named entity 'drug-induced' named entity 'USP18'

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