High rate of proV47A selection in HIV-2 patients failing lopinavir-based HAART.
We describe the emergence of the proV47A mutation in three out of five HIV-2-infected individuals failing lopinavir/ritonavir-based HAART. The appearance of such mutated variants resulted in high levels of phenotypic resistance to lopinavir, cross-resistance to indinavir, amprenavir, and hypersusceptibility to saquinavir. A search in HIV-2 databases revealed that proV47A is present in 8.6% of protease inhibitor (PI)-experienced patients but absent in all PI-naive patients. Its selection may be a common mutational pathway for developing resistance to lopinavir/ritonavir in HIV-2.
Rodés
Berta
B
Molecular Biology Laboratory, Department of Infectious Diseases, Hospital Carlos III, Madrid, Spain.
Toro
Carlos
C
Sheldon
Julie A
JA
Jiménez
Victoria
V
Mansinho
Kamal
K
Soriano
Vincent
V
D000293:Adolescent; D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D024882:Drug Resistance, Viral; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics*; D017320:HIV Protease Inhibitors / Q000627:therapeutic use*; D015498:HIV-2 / Q000235:genetics*; D006801:Humans; D061466:Lopinavir; D008297:Male; D008875:Middle Aged; D009154:Mutation; D010641:Phenotype; D011744:Pyrimidinones / Q000627:therapeutic use*; D019438:Ritonavir / Q000627:therapeutic use; D017211:Treatment Failure
D017320:HIV Protease Inhibitors; D011744:Pyrimidinones; D061466:Lopinavir; D019438:Ritonavir