http://purl.uniprot.org/citations/25115498 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25115498 | http://www.w3.org/2000/01/rdf-schema#comment | "Toll-like receptors (TLRs) and cytoplasmic RNA sensors have been reported to be involved in the regulation of hepatitis B virus (HBV) replication, but remain controversial due to the lack of a natural infectious model. Our current study sets out to characterize aspects of the role of the innate immune system in eliminating HBV using hydrodynamic-based injection of HBV replicative plasmid and knockout mice deficient in specific pathways of the innate system. The evidence indicated that viral replication was not affected by MAVS or TICAM-1 knockout, but absence of interferon regulatory factor 3 (IRF-3) and IRF-7 transcription factors, as well as the interferon (IFN) receptor, had an adverse effect on the inhibition of HBV replication, demonstrating the dispensability of MAVS and TICAM-1 pathways in the early innate response against HBV. Myd88(-/-) mice did not have a significant increase in the initial viremia, but substantial viral antigen persisted in the mice sera, a response similar to Rag2(-/-) mice, suggesting that the MyD88-dependent pathway participated in evoking an adaptive immune response against the clearance of intrahepatic HBV. Taken together, we show that the RNA-sensing pathways do not participate in the regulation of HBV replication in a mouse model; meanwhile MyD88 is implicated in the HBV clearance."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.org/dc/terms/identifier | "doi:10.1159/000365113"xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Matsumoto M."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Okamoto M."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Azuma M."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Seya T."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Chayama K."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Oshiumi H."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Takaki H."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/author | "Leong C.R."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/name | "J Innate Immun"xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/pages | "47-58"xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/title | "A MAVS/TICAM-1-independent interferon-inducing pathway contributes to regulation of hepatitis B virus replication in the mouse hydrodynamic injection model."xsd:string |
http://purl.uniprot.org/citations/25115498 | http://purl.uniprot.org/core/volume | "7"xsd:string |
http://purl.uniprot.org/citations/25115498 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/25115498 |
http://purl.uniprot.org/citations/25115498 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/25115498 |
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http://purl.uniprot.org/uniprot/Q80UF7 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25115498 |
http://purl.uniprot.org/uniprot/Q3U5B1 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25115498 |
http://purl.uniprot.org/uniprot/Q8VCF0 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/25115498 |