pubmed-article:17626094 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0011315 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0598312 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
pubmed-article:17626094 | lifeskim:mentions | umls-concept:C0392760 | lld:lifeskim |
pubmed-article:17626094 | pubmed:issue | 18 | lld:pubmed |
pubmed-article:17626094 | pubmed:dateCreated | 2007-8-30 | lld:pubmed |
pubmed-article:17626094 | pubmed:abstractText | Tumor necrosis factor alpha (TNF-alpha) is believed to play a significant role in the pathogenesis of dengue virus (DV) infection, with elevated levels of TNF-alpha in the sera of DV-infected patients paralleling the severity of disease and TNF-alpha release being coincident with the peak of DV production from infected monocyte-derived macrophages (MDM) in vitro. Since macrophages are a primary cell target in vivo for DV infection, we investigated the potential antiviral role of TNF-alpha in regulating DV replication in MDM. While pretreatment of MDM with TNF-alpha had a minor inhibitory effect, addition of TNF-alpha to MDM with established DV infection had no effect on DV replication as measured by DV RNA levels or progeny virus production. Blocking endogenous TNF-alpha using short interfering RNA or inhibitory TNF-alpha antibodies also had no effect on infectious DV production or viral RNA synthesis. Together, these results demonstrate that DV replication in MDM is not affected by TNF-alpha. Additionally, normal cellular TNF-alpha signaling, measured by quantitation of TNF-alpha-induced stimulation of transcription from an NF-kappaB-responsive reporter plasmid or NF-kappaB protein nuclear translocation, was blocked in DV-infected MDM and Huh7 cells. Thus, DV replication in MDM is not affected by TNF-alpha, and infected cells do not respond normally to TNF-alpha stimulation. It is therefore unlikely that the increased production of TNF-alpha seen in DV infection directly effects DV clearance by reducing DV replication, and the ability of DV to alter TNF-alpha responsiveness highlights another example of viral subversion of cellular functions. | lld:pubmed |
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pubmed-article:17626094 | pubmed:language | eng | lld:pubmed |
pubmed-article:17626094 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17626094 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17626094 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17626094 | pubmed:month | Sep | lld:pubmed |
pubmed-article:17626094 | pubmed:issn | 0022-538X | lld:pubmed |
pubmed-article:17626094 | pubmed:author | pubmed-author:LiPengP | lld:pubmed |
pubmed-article:17626094 | pubmed:author | pubmed-author:BurrellChrist... | lld:pubmed |
pubmed-article:17626094 | pubmed:author | pubmed-author:CarrJillian... | lld:pubmed |
pubmed-article:17626094 | pubmed:author | pubmed-author:WatiSatiyaS | lld:pubmed |
pubmed-article:17626094 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17626094 | pubmed:volume | 81 | lld:pubmed |
pubmed-article:17626094 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17626094 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17626094 | pubmed:pagination | 10161-71 | lld:pubmed |
pubmed-article:17626094 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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