| pubmed-article:8427717 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0020336 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0598312 | lld:lifeskim |
| pubmed-article:8427717 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:8427717 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8427717 | pubmed:dateCreated | 1993-3-5 | lld:pubmed |
| pubmed-article:8427717 | pubmed:abstractText | Chloroquine and its analogue hydroxychloroquine (HCQ) have been shown to inhibit a variety of viral infections including influenza and adenovirus through blockade of viral entry via inhibition of endosomal acidification. We have extended these observations to human immunodeficiency virus type 1 (HIV-1) infection utilizing primary T cells and monocytes, a T cell line (CEM), and a monocytic cell line (U-937). HCQ inhibited HIV-1 replication (> 75%), as measured by reverse transcriptase activity, in the primary T cells and monocytes as well as the T cell and monocytic cell lines. HCQ itself had no anti-reverse transcriptase activity and was not toxic to the cells at concentrations inhibitory to viral replication. Intracytoplasmic staining with an anti-p24 antibody, 24 h after infection, revealed the presence of intracytoplasmic virus, suggesting that the drug does not block viral entry. The production of steady-state HIV-1 mRNA was not affected by HCQ in that comparable levels of HIV-1 mRNA could be detected by Northern blot analysis and by in situ hybridization in both the HCQ-treated and untreated cells. However, HCQ does appear to affect production of infectious HIV-1 virions because viral isolates from HCQ-treated cells could not infect target CEM cells. These data suggest that HCQ may be useful adjunctive therapy in the treatment of HIV-1 infection. | lld:pubmed |
| pubmed-article:8427717 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8427717 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8427717 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8427717 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8427717 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8427717 | pubmed:issn | 0889-2229 | lld:pubmed |
| pubmed-article:8427717 | pubmed:author | pubmed-author:BanerjeeRR | lld:pubmed |
| pubmed-article:8427717 | pubmed:author | pubmed-author:MayerLL | lld:pubmed |
| pubmed-article:8427717 | pubmed:author | pubmed-author:StecherV JVJ | lld:pubmed |
| pubmed-article:8427717 | pubmed:author | pubmed-author:SperberKK | lld:pubmed |
| pubmed-article:8427717 | pubmed:author | pubmed-author:KalbT HTH | lld:pubmed |
| pubmed-article:8427717 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8427717 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:8427717 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8427717 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8427717 | pubmed:pagination | 91-8 | lld:pubmed |
| pubmed-article:8427717 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:meshHeading | pubmed-meshheading:8427717-... | lld:pubmed |
| pubmed-article:8427717 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8427717 | pubmed:articleTitle | Inhibition of human immunodeficiency virus type 1 replication by hydroxychloroquine in T cells and monocytes. | lld:pubmed |
| pubmed-article:8427717 | pubmed:affiliation | Division of Clinical Immunology, Mount Sinai Medical Center, New York, NY 10029. | lld:pubmed |
| pubmed-article:8427717 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8427717 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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