title: Genotypic resistance profile in treatment-experienced HIV-infected individuals after abacavir and efavirenz salvage regimen.
abstract: Once highly active antiretroviral therapy (HAART) fails to suppress HIV replication and resistant viruses emerge, it is difficult to find a salvage regimen since cross-resistance is high among the available classes of antiretroviral drugs. In this retrospective analysis, genotypic resistance profiles were analysed in 24 patients who switched treatment to abacavir (ABV), efavirenz (EFV), and either a NRTI or a PI at baseline and after 24 weeks of treatment. At baseline, 71% of patients harboured at least one resistance mutation in the protease gene. In the RT gene, 87.5% of the patients showed nucleoside analogue resistance mutations, and an equal 87.5% showed resistance mutations to non-nucleoside analogues. After 24 weeks of treatment, only mutations to nucleoside analogues raised in 95.8% of the patients, while resistance mutations to the other drug classes remained constant. Substitutions conferring cross-resistance within each drug family were very common among this treatment-experienced population. These data also indicate that salvage therapy is likely to remain one of the most important issues in the treatment of HIV infections.
authors.affiliation: Grupo de Estudio Hepatitis Viricas y SIDA, Edificio de Laboratorios, 6 Planta, Hospital Universitario Virgen del Rocio, Manuel Siurot s/n, 41013, Seville, Spain. avallejo@cica.es
authors.forename: Alejandro
authors.initials: A
authors.lastname: Vallejo
authors.forename: Mercedes
authors.initials: M
authors.lastname: Olivera
authors.forename: Amalia
authors.initials: A
authors.lastname: Rubio
authors.forename: Armando
authors.initials: A
authors.lastname: Sánchez-Quijano
authors.forename: Eduardo
authors.initials: E
authors.lastname: Lissen
authors.forename: Manuel
authors.initials: M
authors.lastname: Leal
mesh_terms: D000480:Alkynes; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D048588:Benzoxazines; D003521:Cyclopropanes; D015224:Dideoxynucleosides / Q000627:therapeutic use*; D024882:Drug Resistance, Viral / Q000235:genetics; D005838:Genotype; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology*; D016333:HIV Protease / Q000235:genetics; D054303:HIV Reverse Transcriptase / Q000235:genetics; D015497:HIV-1 / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics*; D006801:Humans; D009154:Mutation; D010078:Oxazines / Q000627:therapeutic use*; D016879:Salvage Therapy; D013997:Time Factors; D000099227:Abacavir
chemical_list: D000480:Alkynes; D019380:Anti-HIV Agents; D048588:Benzoxazines; D003521:Cyclopropanes; D015224:Dideoxynucleosides; D016333:HIV Protease; D054303:HIV Reverse Transcriptase; D010078:Oxazines; D000099227:Abacavir; C098320:efavirenz