About: Influenza A Virus Nucleoprotein Exploits Hsp40 to Inhibit PKR Activation

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About: Influenza A Virus Nucleoprotein Exploits Hsp40 to Inhibit PKR Activation 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	Influenza A Virus Nucleoprotein Exploits Hsp40 to Inhibit PKR Activation
Creator	Sambhara, Suryaprakash Sharma, Kulbhushan Deyde, Varough Garten, Rebecca Kumar, Purnima Ranjan, Priya Tripathi, Shashank Katz, Jacqueline Cox, Nancy Lal, Renu Lal, Sunil
Source	Medline; PMC
abstract	BACKGROUND: Double-stranded RNA dependent protein kinase (PKR) is a key regulator of the anti-viral innate immune response in mammalian cells. PKR activity is regulated by a 58 kilo Dalton cellular inhibitor (P58(IPK)), which is present in inactive state as a complex with Hsp40 under normal conditions. In case of influenza A virus (IAV) infection, P58(IPK) is known to dissociate from Hsp40 and inhibit PKR activation. However the influenza virus component responsible for PKR inhibition through P58(IPK) activation was hitherto unknown. PRINCIPAL FINDINGS: Human heat shock 40 protein (Hsp40) was identified as an interacting partner of Influenza A virus nucleoprotein (IAV NP) using a yeast two-hybrid screen. This interaction was confirmed by co-immunoprecipitation studies from mammalian cells transfected with IAV NP expressing plasmid. Further, the IAV NP-Hsp40 interaction was validated in mammalian cells infected with various seasonal and pandemic strains of influenza viruses. Cellular localization studies showed that NP and Hsp40 co-localize primarily in the nucleus. During IAV infection in mammalian cells, expression of NP coincided with the dissociation of P58(IPK) from Hsp40 and decrease PKR phosphorylation. We observed that, plasmid based expression of NP in mammalian cells leads to decrease in PKR phosphorylation. Furthermore, inhibition of NP expression during influenza virus replication led to PKR activation and concomitant increase in eIF2α phosphorylation. Inhibition of NP expression also led to reduced IRF3 phosphorylation, enhanced IFN β production and concomitant reduction of virus replication. Taken together our data suggest that NP is the viral factor responsible for P58(IPK) activation and subsequent inhibition of PKR-mediated host response during IAV infection. SIGNIFICANCE: Our findings demonstrate a novel role of IAV NP in inhibiting PKR-mediated anti-viral host response and help us understand P58(IPK) mediated inhibition of PKR activity during IAV infection.
has issue date	2011-06-15(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0020215
bibo:pmid	21698289
has license	cc0
sha1sum (hex)	93b3fcce1e0a7c9a82091bd832b1b3a286133679
schema:url	https://doi.org/10.1371/journal.pone.0020215
resource representing a document's title	Influenza A Virus Nucleoprotein Exploits Hsp40 to Inhibit PKR Activation
has PubMed Central identifier	PMC3115951
has PubMed identifier	21698289
schema:publication	PLoS One
resource representing a document's body	covid:93b3fcce1e0a7c9a82091bd832b1b3a286133679#body_text
is schema:about of	named entity 'regulated' named entity 'PKR' named entity 'inhibitor' named entity 'INHIBITION' named entity 'TO INHIBIT' named entity 'INFECTION' named entity 'CONDITIONS' named entity 'CASE' named entity 'PKR' named entity 'INFLUENZA A VIRUS' named entity 'INFLUENZA A VIRUS NUCLEOPROTEIN' named entity 'EXPLOITS' named entity 'HSP40' named entity 'KNOWN' named entity 'PROTEIN KINASE' named entity 'ACTIVATION' named entity 'PKR' named entity 'INFLUENZA VIRUS' named entity 'INACTIVE STATE' named entity 'HSP40' named entity 'DOUBLE-STRANDED RNA' named entity 'ACTIVATION' named entity 'INHIBITOR' named entity 'UNKNOWN' named entity 'DALTON' named entity 'PRESENT' named entity 'DEPENDENT' named entity 'VIRAL' named entity 'KEY' named entity 'MAMMALIAN' named entity 'IPK' named entity 'RESPONSIBLE' named entity 'BACKGROUND' named entity 'CELLULAR' named entity 'COMPLEX' named entity 'P58' named entity 'NORMAL' named entity 'REGULATED' named entity 'KILO' named entity 'IS A' named entity 'REGULATOR' named entity 'ACTIVITY' named entity 'INNATE IMMUNE RESPONSE' named entity 'CELLS' named entity 'VIRUS COMPONENT' covid:arg/93b3fcce1e0a7c9a82091bd832b1b3a286133679 named entity 'anti-viral' named entity 'case' named entity 'IPK' named entity 'PKR' named entity 'kilo' named entity 'inhibition' named entity 'influenza virus' named entity 'protein kinase' named entity 'Hsp40' named entity 'Influenza' named entity 'RIG-I' named entity 'DMEM' named entity 'anti-viral' named entity '2, 3' named entity 'Invitrogen' named entity 'IRF3' named entity 'Hsp40' named entity 'Centres for Disease Control and Prevention' named entity 'plasmid' named entity 'RNA' named entity 'mRNAs' named entity 'phosphorylation' named entity 'viral replication' named entity 'Hsp40' named entity 'negative sense'

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