Objective: Although 2 widely used susceptibility assays have been developed, their precision and sensitivity have not been assessed.
Design and Methods: To assess the precision of the Antivirogram and PhenoSense assays, we examined susceptibility results of HIV-1 isolates lacking drug resistance mutations and containing matching patterns of drug resistance mutations. To assess sensitivity, we determined for each assay the proportion of isolates with common patterns of matching drug resistance mutations having reductions in susceptibility greater than those in isolates without drug resistance mutations.
Results: We analyzed protease inhibitor (PI) susceptibility results obtained by the Antivirogram assay for 293 isolates and by the PhenoSense assay for 300 isolates. We analyzed reverse transcriptase (RT) inhibitor susceptibility results obtained by the Antivirogram assay for 202 isolates and by the PhenoSense assay for 126 isolates. For wild-type and mutant isolates, the median absolute deviance of the fold resistance of nucleoside RT inhibitor susceptibility results was significantly lower for the PhenoSense assay than for the Antivirogram assay. The PhenoSense assay was also significantly more likely than the Antivirogram assay to detect resistance to abacavir, didanosine, and stavudine in isolates with the common drug resistance mutations M41L, M184V, and T215Y (±L210W). We found no significant differences between the 2 assays for detecting PI and nonnucleoside RT inhibitor resistance.
Conclusion: The PhenoSense assay is more precise than the Antivirogram assay and superior at detecting resistance to abacavir, didanosine, and stavudine.
From the *Division of Infectious Diseases, Department of Medicine, Stanford University, Stanford, CA; and †Department of Statistics, Stanford University, Stanford, CA.
Received for publication May 15, 2004; accepted September 28, 2004.
J. Zhang and R. W. Shafer were supported in part by a grant from the National Institutes of Allergy and Infectious Diseases (AI46148-01). S.-Y. Rhee, J. Taylor, and R. W. Shafer were supported in part by a grant from the National Institute of General Medical Sciences (5P01GM066524-02).
Reprints: Robert W. Shafer, Division of Infectious Diseases, Room S-169, Stanford University Medical Center, Stanford, CA 94305 (e-mail: firstname.lastname@example.org).