| pubmed-article:9453250 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0009013 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C0213800 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9453250 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:9453250 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9453250 | pubmed:dateCreated | 1998-3-2 | lld:pubmed |
| pubmed-article:9453250 | pubmed:abstractText | Transition from latency to active replication is a crucial stage for the process of human immunodeficiency virus type 1 (HIV-1) infection and life cycle. HIV-1 replication in latently infected cells can be strongly induced by the cytokine tumor necrosis factor alpha (TNF-alpha) and the proliferation-arresting chemical sodium butyrate (NaB). We have investigated the ability of the drug 9-nitrocamptothecin (9NC), a potent cellular topoisomerase I (topo I) inhibitor currently in clinical trials in cancer patients, to regulate HIV-1 replication in latently infected lymphocytic ACH-2 cells on reactivation with either TNF-alpha or NaB. Treatment of ACH-2 cells with 9NC alone resulted in increased levels of viral transcripts, while there was a slight reduction or no change in the levels of host cell transcripts. However, pretreatment of ACH-2 cells with 9NC inhibited TNF-alpha-induced extracellular HIV-1 p24 levels up to approximately 95% and nearly 80% of the cell-associated viral RNAs. The quantitative decrease in viral products was concomitant with a decrease in cellular gene expression and induction of apoptosis in the host cells. 9NC blocked the infected cells at the boundary of the S and G2 phases, resulting in an accelerated apoptosis that was further enhanced with TNF-alpha treatment. Similar results were observed following concurrent exposure to TNF-alpha and 9NC, but 9NC failed to inhibit upregulation of HIV-1 mRNA in ACH-2 cells exposed to TNF-alpha before 9NC treatment. Further, 9NC had no inhibitory effect on NaB-induced apoptosis and upregulation of HIV-1 mRNA expression regardless of whether 9NC and NaB were used concurrently or in various treatment sequences. In uninfected lymphocytic CEM cells derived from a common parental cell line, a slight downregulation of cellular gene expression was detected along with low-level apoptosis. These results demonstrate that 9NC impairs TNF-alpha-induced, but not NaB-induced, HIV-1 activation, and suggest a means of inhibiting active HIV-1 viremia arising as a result of elevated TNF-alpha levels. | lld:pubmed |
| pubmed-article:9453250 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9453250 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9453250 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9453250 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:9453250 | pubmed:issn | 0889-2229 | lld:pubmed |
| pubmed-article:9453250 | pubmed:author | pubmed-author:PantazisPP | lld:pubmed |
| pubmed-article:9453250 | pubmed:author | pubmed-author:EpsteinJ SJS | lld:pubmed |
| pubmed-article:9453250 | pubmed:author | pubmed-author:SadaieM RMR | lld:pubmed |
| pubmed-article:9453250 | pubmed:author | pubmed-author:MoultonSS | lld:pubmed |
| pubmed-article:9453250 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9453250 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9453250 | pubmed:volume | 14 | lld:pubmed |
| pubmed-article:9453250 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9453250 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9453250 | pubmed:pagination | 39-49 | lld:pubmed |
| pubmed-article:9453250 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:meshHeading | pubmed-meshheading:9453250-... | lld:pubmed |
| pubmed-article:9453250 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9453250 | pubmed:articleTitle | 9-Nitrocamptothecin inhibits tumor recrosis factor-mediated activation of human immunodeficiency virus type 1 and enhances apoptosis in a latently infected T cell clone. | lld:pubmed |
| pubmed-article:9453250 | pubmed:affiliation | Division of Transfusion Transmitted Diseases, CBER/Food and Drug Administration, Rockville, Maryland 20852-1448, USA. | lld:pubmed |
| pubmed-article:9453250 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9453250 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9453250 | lld:pubmed |
