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dc.contributor.authorSoria, A
dc.contributor.authorPorten, K
dc.contributor.authorFampou-Toundji, J
dc.contributor.authorGalli, L
dc.contributor.authorMougnutou, R
dc.contributor.authorBuard, V
dc.contributor.authorKfutwah, A
dc.contributor.authorVessière, A
dc.contributor.authorRousset, D
dc.contributor.authorTeck, R
dc.contributor.authorCalmy, A
dc.contributor.authorCiaffi, L
dc.contributor.authorLazzarin, A
dc.contributor.authorGianotti, N
dc.date.accessioned2009-09-20T23:37:36Z
dc.date.available2009-09-20T23:37:36Z
dc.date.issued2009-08
dc.identifier.citationResistance profiles after different periods of exposure to a first-line antiretroviral regimen in a Cameroonian cohort of HIV type-1-infected patients. 2009, 14 (3):339-47 Antivir. Ther. (Lond.)en
dc.identifier.issn1359-6535
dc.identifier.pmid19474468
dc.identifier.urihttp://hdl.handle.net/10144/81753
dc.description.abstractBACKGROUND: The lack of HIV type-1 (HIV-1) viral load (VL) monitoring in resource-limited settings might favour the accumulation of resistance mutations and thus hamper second-line treatment efficacy. We investigated the factors associated with resistance after the initiation of antiretroviral therapy (ART) in the absence of virological monitoring. METHODS: Cross-sectional VL sampling of HIV-1-infected patients receiving first-line ART (nevirapine or efavirenz plus stavudine or zidovudine plus lamivudine) was carried out; those with a detectable VL were genotyped. RESULTS: Of the 573 patients undergoing VL sampling, 84 were genotyped. The mean number of nucleoside/nucleotide reverse transcriptase inhibitor (NRTI) mutations increased with the duration of ART exposure (P=0.02). Multivariable analysis showed that patients with a CD4+ T-cell count < or =50 cells/mm(3) at ART initiation (baseline) had a higher mean number of both NRTI and non-NRTI (NNRTI) mutations than those with a baseline CD4+ T-cell count >50 cells/mm(3) (2.10 versus 0.56; P<0.0001; and 1.65 versus 0.76; P=0.005, respectively). A baseline CD4+ T-cell count < or =50 cells/mm(3) predicted > or =1 NRTI mutation (adjusted odds ratio [AOR] 7.49, 95% confidence interval [CI] 2.20-32.14), > or =1 NNRTI mutation (AOR 4.25, 95% CI 1.36-15.48), > or =1 thymidine analogue mutation (AOR 8.45, 95% CI 2.16-40.16) and resistance to didanosine (AOR 6.36, 95% CI 1.49-32.29) and etravirine (AOR 4.72, 95% CI 1.53-15.70). CONCLUSIONS: Without VL monitoring, the risk of drug resistance increases with the duration of ART and is associated with lower CD4+ T-cell counts at ART initiation. These data might help define strategies to preserve second-line treatment options in resource-limited settings.
dc.language.isoenen
dc.relation.urlhttp://www.intmedpress.comen
dc.rightsArchived on this site with kind permission of International Medical Press. http://www.intmedpress.comen
dc.subject.meshAdulten
dc.subject.meshAnti-HIV Agentsen
dc.subject.meshAntiretroviral Therapy, Highly Activeen
dc.subject.meshCD4 Lymphocyte Counten
dc.subject.meshCameroonen
dc.subject.meshCohort Studiesen
dc.subject.meshCross-Sectional Studiesen
dc.subject.meshDrug Resistance, Multiple, Viralen
dc.subject.meshFemaleen
dc.subject.meshHIV Infectionsen
dc.subject.meshHIV-1en
dc.subject.meshHumansen
dc.subject.meshMaleen
dc.subject.meshMutationen
dc.subject.meshReverse Transcriptase Inhibitorsen
dc.subject.meshViral Loaden
dc.titleResistance profiles after different periods of exposure to a first-line antiretroviral regimen in a Cameroonian cohort of HIV type-1-infected patients.en
dc.contributor.departmentDepartment of Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy. a.soria@hsgerardo.orgen
dc.identifier.journalAntiviral Therapyen
refterms.dateFOA2019-03-04T14:26:39Z
html.description.abstractBACKGROUND: The lack of HIV type-1 (HIV-1) viral load (VL) monitoring in resource-limited settings might favour the accumulation of resistance mutations and thus hamper second-line treatment efficacy. We investigated the factors associated with resistance after the initiation of antiretroviral therapy (ART) in the absence of virological monitoring. METHODS: Cross-sectional VL sampling of HIV-1-infected patients receiving first-line ART (nevirapine or efavirenz plus stavudine or zidovudine plus lamivudine) was carried out; those with a detectable VL were genotyped. RESULTS: Of the 573 patients undergoing VL sampling, 84 were genotyped. The mean number of nucleoside/nucleotide reverse transcriptase inhibitor (NRTI) mutations increased with the duration of ART exposure (P=0.02). Multivariable analysis showed that patients with a CD4+ T-cell count < or =50 cells/mm(3) at ART initiation (baseline) had a higher mean number of both NRTI and non-NRTI (NNRTI) mutations than those with a baseline CD4+ T-cell count >50 cells/mm(3) (2.10 versus 0.56; P<0.0001; and 1.65 versus 0.76; P=0.005, respectively). A baseline CD4+ T-cell count < or =50 cells/mm(3) predicted > or =1 NRTI mutation (adjusted odds ratio [AOR] 7.49, 95% confidence interval [CI] 2.20-32.14), > or =1 NNRTI mutation (AOR 4.25, 95% CI 1.36-15.48), > or =1 thymidine analogue mutation (AOR 8.45, 95% CI 2.16-40.16) and resistance to didanosine (AOR 6.36, 95% CI 1.49-32.29) and etravirine (AOR 4.72, 95% CI 1.53-15.70). CONCLUSIONS: Without VL monitoring, the risk of drug resistance increases with the duration of ART and is associated with lower CD4+ T-cell counts at ART initiation. These data might help define strategies to preserve second-line treatment options in resource-limited settings.


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