Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 203, Issue 9, Pages 1204-1214Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jir025
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Funding
- Merck Laboratories
- GlaxoSmithKline
- Gilead Sciences
- NIH [AI46148, AI068581]
- Spanish Infectious Diseases Society
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With the approval in 2007 of the first integrase inhibitor (INI), raltegravir, clinicians became better able to suppress virus replication in patients infected with human immunodeficiency virus type 1 (HIV-1) who were harboring many of the most highly drug-resistant viruses. Raltegravir also provided clinicians with additional options for first-line therapy and for the simplification of regimens in patients with stable virological suppression. Two additional INIs in advanced clinical development-elvitegravir and S/GSK1349572-may prove equally versatile. However, the INIs have a relatively low genetic barrier to resistance in that 1 or 2 mutations are capable of causing marked reductions in susceptibility to raltegravir and elvitegravir, the most well-studied INIs. This perspective reviews the genetic mechanisms of INI resistance and their implications for initial INI therapy, the treatment of antiretroviral-experienced patients, and regimen simplification.
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