About: Porcine reproductive and respiratory syndrome virus suppresses post-transcriptionally the protein expression of IFN-β by upregulating cellular microRNAs in porcine alveolar macrophages in vitro

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About: Porcine reproductive and respiratory syndrome virus suppresses post-transcriptionally the protein expression of IFN-β by upregulating cellular microRNAs in porcine alveolar macrophages in vitro Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Porcine reproductive and respiratory syndrome virus suppresses post-transcriptionally the protein expression of IFN-β by upregulating cellular microRNAs in porcine alveolar macrophages in vitro
Creator	Zhou, Lei Hu, Dongmei Ge, Xinna Guo, Xin Yang, Hanchun Wang, Lilin
Source	PMC
abstract	Porcine reproductive and respiratory syndrome virus (PRRSV) has been recognized to inhibit the response of type I interferon (IFN) both in vivo and in vitro. However, the post-transcriptional mechanism by which PRRSV suppresses type I IFN induction in virus-infected host cells remains unclear. The present study first demonstrated that PRRSV inhibited post-transcriptionally the protein induction of IFN-β in primary porcine alveolar macrophages (PAMs) during early infection, and the inhibition effect mediated by the Chinese highly pathogenic (HP)-PRRSV was stronger. Next, we analyzed the cellular microRNA (miRNA)-modulated protein expression of porcine IFN-β by dual firefly/Renilla luciferase reporter assay, transfection of miRNA mimics and inhibitor assay and polyinosinic-polycytidylic acid (poly I:C) treatment of PAMs, showing that porcine miRNAs including let-7b, miR-26a, miR-34a and miR-145 are able to inhibit IFN-β protein expression in primary PAMs by directly targeting sequences within the porcine IFN-β 3′UTR locating at 160–181, 9–31, 27–47 and 12–32 bp, respectively. Finally, we confirmed that let-7b, miR-26a, miR-34a and miR-145, were upregulated in PRRSV-infected PAMs early in vitro, and the expression level of these miRNAs in HP-PRRSV JXwn06-infected PAMs were higher than those in low pathogenic PRRSV HB-1/3.9-infected PAMs. The endogenous cellular miRNA-mediated inhibition of IFN-β induction in PRRSV-infected PAMs early could be relieved by miRNA antagonists. Taken together, our findings suggest for the first time that PRRSV can suppress post-transcriptionally protein expression of IFN-β by upregulating cellular miRNAs in PAMs in vitro, providing novel insight into mechanisms in relation to the PRRSV-mediated immunomodulation of porcine innate immunity.
has issue date	2017-10-30(xsd:dateTime)
bibo:doi	10.3892/etm.2017.5397
bibo:pmid	29387185
has license	cc-by-nc-nd
sha1sum (hex)	60bcf8aea7134c49453a05d2b9d52728cc6edcd6
schema:url	https://doi.org/10.3892/etm.2017.5397
resource representing a document's title	Porcine reproductive and respiratory syndrome virus suppresses post-transcriptionally the protein expression of IFN-β by upregulating cellular microRNAs in porcine alveolar macrophages in vitro
has PubMed Central identifier	PMC5769220
has PubMed identifier	29387185
schema:publication	Exp Ther Med
resource representing a document's body	covid:60bcf8aea7134c49453a05d2b9d52728cc6edcd6#body_text
is schema:about of	named entity 'IN VITRO' named entity 'RELIEVED BY' named entity 'TYPE' named entity 'CHINESE' named entity 'PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS' named entity 'EXPRESSION LEVEL' named entity 'TRANSCRIPTIONAL' named entity 'MODULATED' named entity 'OUR' named entity 'LET-7B' named entity 'POLYINOSINIC-POLYCYTIDYLIC ACID' named entity 'IMMUNOMODULATION' named entity 'B2 PROTEIN' named entity 'MIR-26A' named entity 'POST' named entity 'MIRNA' named entity 'STUDY' named entity 'INFECTED' named entity 'INSIGHT' named entity 'PAMS' named entity 'LOW' named entity 'PRESENT' named entity 'PROTEIN ' named entity 'VIRUS' named entity 'ALVEOLAR MACROPHAGES' named entity 'RESPONSE' named entity 'TIME' named entity 'INFECTED HOST' named entity 'ANALYZED' named entity 'PROVIDING' named entity 'THESE' named entity 'porcine' named entity 'relieved' named entity 'dual' named entity 'PAMs' named entity 'post-transcriptional' named entity 'expression' named entity 'expression' named entity 'pathogenic' named entity 'induction' named entity 'ALVEOLAR MACROPHAGES' named entity 'PORCINE' named entity 'UPREGULATED' named entity 'TREATMENT' named entity 'MIRNAS' named entity 'POST' named entity 'CELLULAR' named entity 'TO INHIBIT' named entity 'SUPPRESS' named entity 'SUGGEST' named entity 'MICRORNA' named entity 'PORCINE' named entity 'MICRORNAS' named entity 'IFN' named entity 'PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS' named entity 'SUPPRESSES' named entity 'CELLULAR' named entity 'SUPPRESSES' named entity 'INHIBITION' named entity 'SEQUENCES' named entity 'IFN' named entity 'LUCIFERASE' named entity 'DUAL' named entity 'INFECTION' named entity 'TYPE I INTERFERON' named entity 'DEMONSTRATED' named entity 'INHIBITED' named entity 'MEDIATED' named entity 'MECHANISM' named entity 'CONFIRMED' named entity 'IN VITRO' named entity 'INHIBITOR' named entity 'MIR-34A' named entity 'ANTAGONISTS' named entity 'EFFECT' named entity 'ENDOGENOUS'

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