Lack of protease inhibitor resistance following treatment failure--too good to be true?
- PMID: 23979153
- PMCID: PMC4381281
- DOI: 10.1172/JCI71784
Lack of protease inhibitor resistance following treatment failure--too good to be true?
Abstract
A 29-year-old man with recently diagnosed HIV infection and a CD4 cell count of 225/mm³ began treatment with atazanavir (300 mg), ritonavir (100 mg), emtricitabine (200 mg), and tenofovir (300 mg) daily. For 18 months, he was treatment adherent and his plasma HIV RNA level was below the limit of detection. He then began a relationship with a new partner, who introduced him to methamphetamines. His medication adherence became erratic, and he missed appointments in clinic. Eventually. he was hospitalized for rehabilitation, and he resumed taking his medications on schedule. Following his discharge, he was found to have a plasma HIV RNA level of 11,400 copies/ml. Genotypic resistance testing revealed only an M184V mutation associated with emtricitabine resistance. A decision regarding his next treatment regimen needs to be made.
Comment on
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Multi-step inhibition explains HIV-1 protease inhibitor pharmacodynamics and resistance.J Clin Invest. 2013 Sep;123(9):3848-60. doi: 10.1172/JCI67399. Epub 2013 Aug 27. J Clin Invest. 2013. PMID: 23979165 Free PMC article.
References
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- Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in the treatment of HIV-1-infected adults and adolescents. Department of Health and Human Services Web site. http://aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf . Accessed June 27, 2013.
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- Eron J, et al. The KLEAN study of fosamprenavir-ritonavir versus lopinavir-ritonavir, each in combination with abacavir-lamivudine, for initial treatment of HIV infection over 48 weeks: a randomized non-inferiority trial. Lancet. 2006;368(9534):476–482. doi: 10.1016/S0140-6736(06)69155-1. - DOI - PubMed
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