pubmed-article:11880402 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C1257890 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C0030946 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C0033607 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C0042333 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C0006802 | lld:lifeskim |
pubmed-article:11880402 | lifeskim:mentions | umls-concept:C2348519 | lld:lifeskim |
pubmed-article:11880402 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:11880402 | pubmed:dateCreated | 2002-3-6 | lld:pubmed |
pubmed-article:11880402 | pubmed:abstractText | To establish a baseline for monitoring resistance to protease inhibitors (PIs) and examining the efficacy of their use among persons in Cameroon infected with human immunodeficiency virus type 1 (HIV-1), we analyzed genetic variability and PI resistance-associated substitutions in PCR-amplified protease (PR) sequences in strains isolated from 110 HIV-1-infected, drug-naïve Cameroonians. Of the 110 strains, 85 were classified into six HIV-1 PR subtypes, A (n = 1), B (n = 1), F (n = 4), G (n = 7), H (n = 1), and J (n = 7), and a circulating recombinant form, CRF02-AG (n = 64). PR genes from the remaining 25 (23%) specimens were unclassifiable, whereas 2% (7 of 301) unclassifiable PR sequences were reported for a global collection. Two major PI resistance-associated mutations, 20M and 24I, were detected in strains from only two specimens, whereas secondary mutations were found in strains from all samples except one strain of subtype B and two strains of CRF02-AG. The secondary mutations showed the typical PI resistance-associated pattern for non-subtype B viruses in both classifiable and unclassifiable PR genes, with 36I being the predominant (99%) mutation, followed by 63P (18%), 20R (15%), 77I (13%), and 10I or 10V (11%). Of these mutations, dual and triple PI resistance-associated substitutions were found in 38% of all the Cameroonian strains. Compared with classifiable PR sequences, unclassifiable sequences had significantly more dual and triple substitutions (64% versus 30%; P = 0.004). Phenotypic and clinical evaluations are needed to estimate whether PI resistance during antiretroviral drug treatment occurs more rapidly in individuals infected with HIV-1 strains harboring multiple PI resistance-associated substitutions. This information may be important for determination of appropriate drug therapies for HIV-1-infected persons in Cameroon, where more than one-third of HIV-1 strains were found to carry dual and triple minor PI resistance-associated mutations. | lld:pubmed |
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pubmed-article:11880402 | pubmed:language | eng | lld:pubmed |
pubmed-article:11880402 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11880402 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:11880402 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11880402 | pubmed:month | Mar | lld:pubmed |
pubmed-article:11880402 | pubmed:issn | 0095-1137 | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:LalRenu BRB | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:NkengasongJoh... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:FonjungoPeter... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:MpoudiEitel... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:TorimiroJudit... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:AlemnjiGeorge... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:EnoLaura TLT | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:LyongaEsther... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:RayfieldMarkM | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:KalishMarcia... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:FolksThomas... | lld:pubmed |
pubmed-article:11880402 | pubmed:author | pubmed-author:PieniazekDanu... | lld:pubmed |
pubmed-article:11880402 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11880402 | pubmed:volume | 40 | lld:pubmed |
pubmed-article:11880402 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11880402 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11880402 | pubmed:pagination | 837-45 | lld:pubmed |
pubmed-article:11880402 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:11880402 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11880402 | pubmed:articleTitle | Human immunodeficiency virus type 1 group m protease in cameroon: genetic diversity and protease inhibitor mutational features. | lld:pubmed |
pubmed-article:11880402 | pubmed:affiliation | HIV and Retrovirology Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases, Atlanta, Georgia 30333, USA. | lld:pubmed |
pubmed-article:11880402 | pubmed:publicationType | Journal Article | lld:pubmed |
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