HIV resistance testing: Difference between revisions
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==Overview== | ==Overview== | ||
The emergence of resistance to one or more antiretroviral drugs is one of the more common reasons for therapeutic failure in the treatment of HIV. In addition, the emergence of resistance to one antiretroviral drug sometimes confers a reduction in or a loss of susceptibility to other or all drugs of the same class. The application of laboratory technologies, such as gene [[amplification]], automated nucleic acid [[sequencing]], and nucleic acid [[hybridization]], and the availability of [[recombinant ]]viruses for testing phenotypic susceptibility have permitted advances in HIV resistance testing. Many clinicians and investigators are currently using these technologies in the clinical management of HIV. | The emergence of resistance to one or more antiretroviral drugs is one of the more common reasons for therapeutic failure in the treatment of HIV. In addition, the emergence of resistance to one antiretroviral drug sometimes confers a reduction in or a loss of susceptibility to other or all drugs of the same class. The application of laboratory technologies, such as gene [[amplification]], automated nucleic acid [[sequencing]], and nucleic acid [[hybridization]], and the availability of [[recombinant ]]viruses for testing phenotypic susceptibility have permitted advances in HIV resistance testing. Many clinicians and investigators are currently using these technologies in the clinical management of HIV. | ||
==Advantage== | |||
Despite limitations of resistance assays and their interpretation, several randomized controlled studies have demonstrated that virologic outcome, at least over the short term, may be improved when genotypic or phenotypic data are used to guide choice of drug regimens in patients with loss of virologic response to prior regimens | |||
==Limitations== | ==Limitations== | ||
*Performance characteristics (e.g., sensitivity, specificity, and reproducibility) for many of the assays in investigational use have not been fully established. | *Performance characteristics (e.g., sensitivity, specificity, and reproducibility) for many of the assays in investigational use have not been fully established. | ||
*The clinical significance of many mutations or mutational patterns has not been defined completely for many antiretroviral drugs. | *The clinical significance of many mutations or mutational patterns has not been defined completely for many antiretroviral drugs. | ||
*The quantitative relationship between reductions of cell culture susceptibility and loss of clinical activity has not been established for most drugs. | *The quantitative relationship between reductions of cell culture susceptibility and loss of clinical activity has not been established for most drugs. |
Revision as of 20:56, 30 May 2012
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Overview
The emergence of resistance to one or more antiretroviral drugs is one of the more common reasons for therapeutic failure in the treatment of HIV. In addition, the emergence of resistance to one antiretroviral drug sometimes confers a reduction in or a loss of susceptibility to other or all drugs of the same class. The application of laboratory technologies, such as gene amplification, automated nucleic acid sequencing, and nucleic acid hybridization, and the availability of recombinant viruses for testing phenotypic susceptibility have permitted advances in HIV resistance testing. Many clinicians and investigators are currently using these technologies in the clinical management of HIV.
Advantage
Despite limitations of resistance assays and their interpretation, several randomized controlled studies have demonstrated that virologic outcome, at least over the short term, may be improved when genotypic or phenotypic data are used to guide choice of drug regimens in patients with loss of virologic response to prior regimens
Limitations
- Performance characteristics (e.g., sensitivity, specificity, and reproducibility) for many of the assays in investigational use have not been fully established.
- The clinical significance of many mutations or mutational patterns has not been defined completely for many antiretroviral drugs.
- The quantitative relationship between reductions of cell culture susceptibility and loss of clinical activity has not been established for most drugs.