pubmed-article:10691920 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0019693 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0021081 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0887947 | lld:lifeskim |
pubmed-article:10691920 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:10691920 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:10691920 | pubmed:dateCreated | 2000-4-24 | lld:pubmed |
pubmed-article:10691920 | pubmed:abstractText | Interferons play an important, but incompletely understood role in HIV-related disease. We investigated the effect of HAART on plasma levels of IFN-alpha, IFN-gamma, neopterin and interferon-inducible protein 10 (IP-10) in 41 HIV-infected patients during 78 weeks of therapy. At baseline HIV-infected patients had raised levels of both IP-10 and IFN-alpha compared with healthy controls (n = 19), with particularly high levels in advanced disease. HAART induced a marked decrease in levels of both IFN-alpha, neopterin and IP-10, though not to normal concentrations. In contrast, IFN-gamma levels were low throughout the study, and not different from controls. While neopterin and IP-10 remained significantly decreased compared with baseline levels throughout the study, IFN-alpha levels returned to baseline at the end of the study. Persistently high IP-10 and IFN-alpha levels were associated with immunological treatment failure and even high baseline levels of IFN-alpha appeared to predict immunological relapse. Furthermore, we found a markedly suppressive effect of exogenously added IFN-alpha on phytohaemagglutinin-stimulated lymphocyte proliferation in both patients and controls, and this suppressive effect seemed not to involve enhanced lymphocyte apoptosis. Our findings suggest a pathogenic role of IFN-alpha in HIV infection, which may be a potential target for immunomodulating therapy in combination with HAART. | lld:pubmed |
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pubmed-article:10691920 | pubmed:language | eng | lld:pubmed |
pubmed-article:10691920 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10691920 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10691920 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10691920 | pubmed:month | Mar | lld:pubmed |
pubmed-article:10691920 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:10691920 | pubmed:author | pubmed-author:MüllerFF | lld:pubmed |
pubmed-article:10691920 | pubmed:author | pubmed-author:BendtzenKK | lld:pubmed |
pubmed-article:10691920 | pubmed:author | pubmed-author:FrølandS SSS | lld:pubmed |
pubmed-article:10691920 | pubmed:author | pubmed-author:AukrustPP | lld:pubmed |
pubmed-article:10691920 | pubmed:author | pubmed-author:StylianouEE | lld:pubmed |
pubmed-article:10691920 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10691920 | pubmed:volume | 119 | lld:pubmed |
pubmed-article:10691920 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10691920 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10691920 | pubmed:pagination | 479-85 | lld:pubmed |
pubmed-article:10691920 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10691920 | pubmed:meshHeading | pubmed-meshheading:10691920... | lld:pubmed |
pubmed-article:10691920 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10691920 | pubmed:articleTitle | Interferons and interferon (IFN)-inducible protein 10 during highly active anti-retroviral therapy (HAART)-possible immunosuppressive role of IFN-alpha in HIV infection. | lld:pubmed |
pubmed-article:10691920 | pubmed:affiliation | Section of Clinical Immunology and Infectious Diseases and Research Institute for Internal Medicine, Medical Department, Rikshospitalet, Oslo, Norway. eva.stylianou@klinmed.uio.no | lld:pubmed |
pubmed-article:10691920 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10691920 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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