About: Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation From Latency by Preventing Virus-induced Systemic Inflammation

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About: Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation From Latency by Preventing Virus-induced Systemic Inflammation 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	Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation From Latency by Preventing Virus-induced Systemic Inflammation
Creator	Zhang, Xin Akira, Shizuo Saitoh, Tatsuya He, You-Wen Guan, Jun-Lin Levine, Beth Martinez, Jennifer Artyomov, Maxim Blackman, Marcia Buck, Michael Desai, Chandni Freeman, Michael Green, Douglas Handley, Scott Loginicheva, Ekaterina Park, Sunmin Reese, Tiffany Virgin, Herbert
Source	Elsevier; Medline; PMC
abstract	Host genes that regulate systemic inflammation upon chronic viral infection are incompletely understood. Murine γ-herpesvirus 68 (MHV68) infection is characterized by latency in macrophages, and reactivation is inhibited by Interferon-γ (IFN-γ). Using a Lysozyme-M-cre (LysMcre) expression system, we show that deletion of autophagy-related (Atg) genes Fip200, beclin 1, Atg14, Atg16L1, Atg7, Atg3, and Atg5, in the myeloid compartment, inhibited MHV68 reactivation in macrophages. Atg5-deficiency did not alter reactivation from B cells, and effects on reactivation from macrophages were not explained by alterations in productive viral replication or the establishment of latency. Rather, chronic MHV68 infection triggered increased systemic inflammation, increased T cell production of IFN-γ and an IFN-γ-induced transcriptional signature in macrophages from Atg gene-deficient mice. The Atg5-related reactivation defect was partially reversed by neutralization of IFN-γ. Thus Atg genes in myeloid cells dampen virus-induced systemic inflammation, creating an environment that fosters efficient MHV68 reactivation from latency.
has issue date	2016-01-01(xsd:dateTime)
bibo:doi	10.1016/j.chom.2015.12.010
bibo:pmid	26764599
has license	hybrid-oa
sha1sum (hex)	385cc928ffabea9239730aac852bfe6cfb877c38
schema:url	https://doi.org/10.1016/j.chom.2015.12.010
resource representing a document's title	Autophagy Genes Enhance Murine Gammaherpesvirus 68 Reactivation From Latency by Preventing Virus-induced Systemic Inflammation
has PubMed Central identifier	PMC4714357
has PubMed identifier	26764599
schema:publication	Cell Host & Microbe
resource representing a document's body	covid:385cc928ffabea9239730aac852bfe6cfb877c38#body_text
is schema:about of	named entity 'vivo' named entity 'ATCC' named entity 'IN VIVO' named entity 'VIRUS' named entity 'LOH' named entity 'OVALBUMIN' named entity 'USED' named entity 'DRIVEN' named entity 'REFERRED TO' named entity 'AUTOPHAGY' named entity 'SPECIFIC' named entity 'ENHANCE' named entity 'GENES' named entity 'LATENCY' named entity 'INDUCED' named entity 'REACTIVATION' named entity 'MURINE GAMMAHERPESVIRUS 68' named entity 'PROMOTER' named entity 'VIRAL' named entity 'REPLICATION' named entity 'SIINFEKL PEPTIDE' named entity 'WILD-TYPE' named entity 'INFECTIONS' named entity 'PREVENTING' named entity 'FIREFLY LUCIFERASE' named entity 'VIRUS' named entity 'STUDY' named entity 'SYSTEMIC INFLAMMATION' named entity 'T CELL' named entity '2012' named entity 'promoter' named entity '2005' named entity 'Genes' named entity 'ova' named entity 'firefly luciferase' named entity 'Systemic Inflammation' named entity 'Virus' named entity 'CD11b' named entity 'cDNA' named entity 'DMEM' named entity 'Mx1' named entity 'Actb' named entity 'F4/80' named entity 'Promega' named entity 'IFN-γ' named entity 'flow cytometry' named entity 'Oasl2' named entity 'genome annotation' named entity 'β-actin' named entity 'gene' named entity 'Trizol' named entity 'barcode' named entity 'macrophages' named entity 'Sidak' named entity 'Gene set enrichment analysis' named entity 'genome annotation' named entity 'staining' named entity 'exons' named entity 'methylcellulose' named entity 'gene' named entity 'internal control' named entity 'silica' named entity 'flow cytometry' named entity 'Invitrogen'

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