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About:
Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation
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schema:ScholarlyArticle
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wasabi.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
title
Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation
Creator
Li, Jie
Liu, Shuai
Qian, Zhikang
Jia, Ran
Speck, Samuel
Wang, Liu
Gao, Ying
Jiang, Congwei
Kuang, Linlin
Lei, Zhangmengxue
Liangid, Xiaozhen
Liu, Mu
Liu, Zhongshun
Zhouid, Dongming
topic
covid:51421e94622c391902ad609d9bfaa85f533e20fe#this
source
Medline; PMC
abstract
Gammaherpesviruses have evolved various strategies to take advantage of host cellular factors or signaling pathways to establish a lifelong latent infection. Like the human gammaherpesvirus Epstein-Barr virus, murine gammaherpesvirus 68 (MHV68) establishes and maintains latency in the memory B cells during infection of laboratory mice. We have previously shown that MHV68 can immortalize fetal liver-derived B cells that induce lymphomas when injected into immunodeficient mice. Here we identify interleukin 16 (IL16) as a most abundantly expressed cytokine in MHV68-immortalized B cells and show that MHV68 infection elevates IL16 expression. IL16 is not important for MHV68 lytic infection but plays a critical role in MHV68 reactivation from latency. IL16 deficiency increases MHV68 lytic gene expression in MHV68-immortalized B cells and enhances reactivation from splenic latency. Correlatively, IL16 deficiency increases the frequency of MHV68-infected plasma cells that can be attributed to enhanced MHV68 reactivation. Furthermore, similar to TPA-mediated lytic replication of Kaposi's sarcoma-associated herpesvirus, IL16 deficiency markedly induces Tyr705 STAT3 de-phosphorylation and elevates p21 expression, which can be counteracted by the tyrosine phosphatase inhibitor orthovanadate. Importantly, orthovanadate strongly blocks MHV68 lytic gene expression mediated by IL16 deficiency. These data demonstrate that virus-induced IL16 does not directly participate in MHV68 lytic replication, but rather inhibits virus reactivation to facilitate latent infection, in part through the STAT3-p21 axis.
has issue date
2020-07-31
(
xsd:dateTime
)
bibo:doi
10.1371/journal.ppat.1008701
bibo:pmid
32735617
has license
cc-by
sha1sum (hex)
51421e94622c391902ad609d9bfaa85f533e20fe
schema:url
https://doi.org/10.1371/journal.ppat.1008701
resource representing a document's title
Interleukin 16 contributes to gammaherpesvirus pathogenesis by inhibiting viral reactivation
has PubMed Central identifier
PMC7423151
has PubMed identifier
32735617
schema:publication
PLoS Pathog
resource representing a document's body
covid:51421e94622c391902ad609d9bfaa85f533e20fe#body_text
is
http://vocab.deri.ie/void#inDataset
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proxy:http/ns.inria.fr/covid19/51421e94622c391902ad609d9bfaa85f533e20fe
is
schema:about
of
named entity 'B cells'
named entity 'lytic'
named entity 'fetal'
named entity 'critical role'
named entity 'maintains'
named entity 'elevates'
named entity 'data'
named entity 'immortalized'
named entity 'inhibiting'
named entity 'Interleukin 16'
named entity 'interleukin'
named entity 'gene'
named entity 'plasma cells'
named entity 'murine'
named entity 'blocks'
named entity 'frequency'
named entity 'infection'
named entity 'host'
named entity 'STAT3'
named entity 'mice'
named entity 'viral'
named entity 'IL16'
named entity 'latent infection'
named entity 'virus'
named entity 'Gammaherpesviruses'
named entity 'IL16'
named entity 'virus'
named entity 'interleukin 16'
named entity 'p21'
named entity 'latent infection'
named entity 'lymphomas'
named entity 'cytokine'
named entity 'gene expression'
named entity 'Epstein-Barr virus'
named entity 'memory B cells'
named entity 'injected'
named entity 'Addgene'
named entity 'amino acid'
named entity 'JAK-STAT'
named entity 'infection'
named entity 'intranasally'
named entity 'APC'
named entity 'IL16'
named entity 'IL16'
named entity 'transfected'
named entity 'CD3'
named entity 'HIV-1'
named entity 'endogenous'
named entity 'cloned'
named entity 'expression profiling'
named entity 'IL16'
named entity 'IL16'
named entity 'supernatant'
named entity 'lentiviral'
named entity 'gene expression'
named entity 'Institut Pasteur'
named entity 'IL16'
named entity 'IL16'
named entity 'IL16'
named entity 'lytic'
named entity 'STAT3'
named entity 'primers'
named entity 'IL16'
named entity 'gene'
named entity 'infection'
named entity 'IL16'
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