About: Zinc Chelation Specifically Inhibits Early Stages of Dengue Virus Replication by Activation of NF-κB and Induction of Antiviral Response in Epithelial Cells

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About: Zinc Chelation Specifically Inhibits Early Stages of Dengue Virus Replication by Activation of NF-κB and Induction of Antiviral Response in Epithelial Cells Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Zinc Chelation Specifically Inhibits Early Stages of Dengue Virus Replication by Activation of NF-κB and Induction of Antiviral Response in Epithelial Cells
Creator	Shi, Lei Kitazawa, Haruki Basak, Soumen Goel, Renu Kar, Meenakshi Panwar, Aleksha Sopory, Shailaja Khan, Ahmed Medigeshi, Guruprasad Bais, Sachendra
topic	covid:e8ae86b48db5e9860652f9c78c61f13c1b41c700#this
Source	Medline; PMC
abstract	Zinc is an essential micronutrient which regulates diverse physiological functions and has been shown to play a crucial role in viral infections. Zinc has a necessary role in the replication of many viruses, however, antiviral action of zinc has also been demonstrated in in vitro infection models most likely through induction of host antiviral responses. Therefore, depending on the host machinery that the virus employs at different stages of infection, zinc may either facilitate, or inhibit virus infection. In this study, we show that zinc plays divergent roles in rotavirus and dengue virus infections in epithelial cells. Dengue virus infection did not perturb the epithelial barrier functions despite the release of virus from the basolateral surface whereas rotavirus infection led to disruption of epithelial junctions. In rotavirus infection, zinc supplementation post-infection did not block barrier disruption suggesting that zinc does not affect rotavirus life-cycle or protects epithelial barriers post-infection suggesting the involvement of cellular pathways in the beneficial effect of zinc supplementation in enteric infections. Zinc depletion by N,N,N',N'-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN) inhibited dengue virus and Japanese encephalitis virus (JEV) infection but had no effect on rotavirus. Time-of-addition experiments suggested that zinc chelation affected both early and late stages of dengue virus infectious cycle and zinc chelation abrogated dengue virus RNA replication. We show that transient zinc chelation induces ER stress and antiviral response by activating NF-kappaB leading to induction of interferon signaling. These results suggest that modulation of zinc homeostasis during virus infection could be a component of host antiviral response and altering zinc homeostasis may act as a potent antiviral strategy against flaviviruses.
has issue date	2019-10-01(xsd:dateTime)
bibo:doi	10.3389/fimmu.2019.02347
bibo:pmid	31632411
has license	cc-by
sha1sum (hex)	e8ae86b48db5e9860652f9c78c61f13c1b41c700
schema:url	https://doi.org/10.3389/fimmu.2019.02347
resource representing a document's title	Zinc Chelation Specifically Inhibits Early Stages of Dengue Virus Replication by Activation of NF-κB and Induction of Antiviral Response in Epithelial Cells
has PubMed Central identifier	PMC6779808
has PubMed identifier	31632411
schema:publication	Front Immunol
resource representing a document's body	covid:e8ae86b48db5e9860652f9c78c61f13c1b41c700#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/e8ae86b48db5e9860652f9c78c61f13c1b41c700
is schema:about of	named entity 'ACTIVATION' named entity 'BAB' named entity 'JEV' named entity 'rotavirus' named entity 'dengue virus' named entity 'play' named entity 'perturb' named entity 'infections' named entity 'NF-κB' named entity 'VIRUS REPLICATION' named entity 'EPITHELIAL CELLS' covid:arg/e8ae86b48db5e9860652f9c78c61f13c1b41c700 named entity 'DENGUE VIRUS' named entity 'ZINC' named entity 'NO EFFECT' named entity 'ACTIVATING' named entity 'RESULTS' named entity 'VIRUS INFECTION' named entity 'VIRUS' named entity 'FLAVIVIRUSES' named entity 'ANTIVIRAL ACTION' named entity 'MODULATION' named entity 'PLAYS' named entity 'INTERFERON SIGNALING' named entity 'DOES NOT' named entity 'TIME' named entity 'MICRONUTRIENT' named entity 'THESE' named entity 'MACHINERY' named entity 'EXPERIMENTS' named entity 'BARRIER' named entity 'MOST LIKELY' named entity 'BLOCK' named entity 'ROLES' named entity 'LATE STAGES' named entity 'DEMONSTRATED' named entity 'BUT' named entity 'INVOLVEMENT' named entity 'PATHWAYS' named entity 'DENGUE VIRUS INFECTION' named entity 'DENGUE VIRUS RNA' named entity 'EPITHELIAL' named entity 'COULD BE' named entity 'RNA REPLICATION' named entity 'ZINC DEPLETION' named entity 'OF-' named entity 'ACT' named entity 'NECESSARY' named entity 'LED' named entity 'ANTIVIRAL RESPONSE' named entity 'IN VITRO' named entity 'ZINC CHELATION' named entity 'CYCLE' named entity 'EPITHELIAL CELLS' named entity 'PHYSIOLOGICAL' named entity 'REPLICATION' named entity 'EARLY STAGES' named entity 'LIFE-CYCLE' named entity 'ZINC HOMEOSTASIS' named entity 'ZINC SUPPLEMENTATION' named entity 'ROTAVIRUS' named entity 'AFFECTED' named entity 'EITHER' named entity 'INFECTIOUS' named entity 'TRANSIENT' named entity 'VIRUSES' named entity 'INFECTIONS' named entity 'INHIBITED' named entity 'AFFECT' named entity 'SURFACE'

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