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Updated September 20, 2006

Case 3: Resistance to Non-Nucleoside Reverse Transcriptase Inhibitors

Authors: Christopher Behrens, MD David H. Spach, MD

A 32-year-old man with a baseline CD4 count of 310 cells/mm3 and HIV RNA level of 45,000 copies/mL initiates antiretroviral therapy with a once-daily regimen of tenofovir DF (Viread) plus didanosine (Videx EC) plus efavirenz (Sustiva). Within 5 months, he has an undetectable HIV RNA. Six months later, however, he has intermittent problems with adherence and develops virologic breakthrough with an HIV RNA level of 5,340 copies/mL. A genotypic resistance assay is performed that shows a K103N mutation in reverse transcriptase and no significant mutations in protease. The patient stops his antiretroviral medications. At a visit one year later, his CD4 count has declined to 227 cells/mm3 and he states he is interested in restarting antiretroviral therapy. A second genotypic resistance assay is performed (not on therapy) and this resistance assay does not show any mutations in reverse transcriptase or protease. The patient has never taken nevirapine (Viramune) or delavirdine (Rescriptor).

Which one of the following statements is TRUE regarding a new salvage regimen for the patient?

A The patient is not likely to have a significant virologic response to efavirenz or nevirapine.
B Although the K103N mutation reflects resistance to efavirenz, the patient should have an excellent virologic response to nevirapine.
C Although the K103N mutation reflects resistance to efavirenz, the patient should have an excellent virologic response to delavirdine.
D If the patient is placed back on efavirenz and the K103N mutation remerges, efavirenz should be continued because the presence of the K103N mutation will markedly reduce viral fitness.